<?xml version="1.0"?>
<?mso-application progid="Excel.Sheet"?>
<Workbook xmlns="urn:schemas-microsoft-com:office:spreadsheet"
 xmlns:o="urn:schemas-microsoft-com:office:office"
 xmlns:x="urn:schemas-microsoft-com:office:excel"
 xmlns:ss="urn:schemas-microsoft-com:office:spreadsheet"
 xmlns:html="http://www.w3.org/TR/REC-html40">
 <DocumentProperties xmlns="urn:schemas-microsoft-com:office:office">
  <Author>wxy</Author>
  <LastAuthor>wxy</LastAuthor>
  <Created>2020-02-21T15:25:01Z</Created>
  <Version>16.00</Version>
 </DocumentProperties>
 <OfficeDocumentSettings xmlns="urn:schemas-microsoft-com:office:office">
  <AllowPNG/>
 </OfficeDocumentSettings>
 <ExcelWorkbook xmlns="urn:schemas-microsoft-com:office:excel">
  <WindowHeight>6770</WindowHeight>
  <WindowWidth>19200</WindowWidth>
  <WindowTopX>32767</WindowTopX>
  <WindowTopY>32767</WindowTopY>
  <ProtectStructure>False</ProtectStructure>
  <ProtectWindows>False</ProtectWindows>
 </ExcelWorkbook>
 <Styles>
  <Style ss:ID="Default" ss:Name="Normal">
   <Alignment ss:Vertical="Center"/>
   <Borders/>
   <Font ss:FontName="等线" x:CharSet="134" ss:Size="11" ss:Color="#000000"/>
   <Interior/>
   <NumberFormat/>
   <Protection/>
  </Style>
 </Styles>
 <Worksheet ss:Name="Sheet1">
  <Table ss:ExpandedColumnCount="6" ss:ExpandedRowCount="1107" x:FullColumns="1"
   x:FullRows="1" ss:DefaultColumnWidth="52" ss:DefaultRowHeight="14">
   <Row>
    <Cell><Data ss:Type="String">Gene  symble</Data></Cell>
    <Cell><Data ss:Type="String">Title</Data></Cell>
    <Cell><Data ss:Type="String">Curated description</Data></Cell>
    <Cell><Data ss:Type="String">Category</Data></Cell>
    <Cell><Data ss:Type="String">Literature category</Data></Cell>
    <Cell><Data ss:Type="String">Pubmed ID</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ABCB1</Data></Cell>
    <Cell><Data ss:Type="String">Exosomes mediate drug resistance transfer in MCF7 breast cancer cells and a probable mechanism is delivery of P-glycoprotein</Data></Cell>
    <Cell><Data ss:Type="String">Exosomes are effective in transferring drug resistance as well as P-gp from drug-resistant breast cancer cells to sensitive ones. The delivery of P-gp via exosomes may be a mechanism of exosome-mediated drug resistance transfer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">25077924</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ABCB1</Data></Cell>
    <Cell><Data ss:Type="String">Polymorphisms in the BRCA1 and ABCB1 genes modulate menopausal hormone therapy associated breast cancer risk in postmenopausal women</Data></Cell>
    <Cell><Data ss:Type="String">Genetic variants in ABCB1 and BRCA1 may modify the effect of Menopausal hormone therapy(HT) on postmenopausal breast cancer risk.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19672706</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ABCB1</Data></Cell>
    <Cell><Data ss:Type="String">Influence of pharmacogenetics on response and toxicity in breast cancer patients treated with doxorubicin and cyclophosphamide</Data></Cell>
    <Cell><Data ss:Type="String">Variant alleles in the ABCB1, SLC22A16 and CYP2B6 genes are associated with response to Doxorubicin and cyclophosphamide(AC) therapy in the treatment of breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">20179710</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ABCB1</Data></Cell>
    <Cell><Data ss:Type="String">The effect of ABCB1 polymorphisms on the outcome of breast cancer treatment</Data></Cell>
    <Cell><Data ss:Type="String">ABCB1 gene may be potential candidate in pharmacogenetic evaluation of breast cancer treatment outcomes and optimizing individualized therapy.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27175090</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ABCB1</Data></Cell>
    <Cell><Data ss:Type="String">The effect of ABCB1 polymorphisms on the outcome of breast cancer treatment</Data></Cell>
    <Cell><Data ss:Type="String">ABCB1 is highly polymorphic, and three well-known single-nucleotide polymorphisms such as 1236C&gt;T, 2677G&gt;T/A, and 3435C&gt;T have been found to be associated with altered messenger RNA levels, protein folding, and drug pharmacokinetics.And these polymorphisms are found to be correlated with phenotypic variation in P-gp expression levels of various tissues.P-gp is widely expressed in the tissues essential in drug disposition such as the intestinal epithelium, adrenal glands, canalicular membrane of the hepatocytes of the liver, kidney proximal tubules, and blood鈥揵rain barrier.Major functions of P-gp proteins include the transport of drugs such as colchicine, tacrolimus, and quinidine; chemotherapeutic agents such as etoposide, doxorubicin, taxol, and vinblastine; and various lipids, bile salts, toxic compounds, and peptides for antigen presentation across the membranes. </Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27175090</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ABCB1</Data></Cell>
    <Cell><Data ss:Type="String">ABCB1 and ABCC11 confer resistance to eribulin in breast cancer cell lines</Data></Cell>
    <Cell><Data ss:Type="String">ABCB1 and ABCC11 expression may be used as a biomarker for predicting the response to eribulin in patients with breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27588398</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ABCB1</Data></Cell>
    <Cell><Data ss:Type="String">Loss of constitutive ABCB1 expression in breast cancer associated with worse prognosis</Data></Cell>
    <Cell><Data ss:Type="String">The loss of constitutive ABCB1 expression in breast cancer, especially in triple-negative tumors, seems to indicate a subgroup of worse prognosis.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28670140</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ABCB1</Data></Cell>
    <Cell><Data ss:Type="String">Development of high resolution melting analysis for ABCB1 promoter methylation: Clinical consequences in breast and ovarian carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">Our data suggest the existence of functional epigenetic changes in the ABCB1 gene with prognostic value in tumor tissues of patients with breast and ovarian carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31173253</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ABCB11</Data></Cell>
    <Cell><Data ss:Type="String">Description of two new ABCB11 mutations responsible for type 2 benign recurrent intrahepatic cholestasis in a French-Canadian family</Data></Cell>
    <Cell><Data ss:Type="String">The present report describes two individuals from the same family whose symptoms were typical of the clinical characteristics of type 2 benign recurrent intrahepatic cholestasis. Sequencing of the?ABCB11?gene revealed two previously unreported mutations that predict the absence of expression of the protein</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21766090</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ABCB11</Data></Cell>
    <Cell><Data ss:Type="String">The role of ABC transporters in progression and clinical outcome of colorectal cancer</Data></Cell>
    <Cell><Data ss:Type="String">ABCC11 may be a promising candidate marker for a validation study on 5-FU therapy outcome</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22294766</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ABCB11</Data></Cell>
    <Cell><Data ss:Type="String">Paediatric hepatocellular carcinoma due to somatic CTNNB1 and NFE2L2 mutations in the setting of inherited bi-allelic ABCB11 mutations</Data></Cell>
    <Cell><Data ss:Type="String">This is the first study to identify somatic CTNNB1 and NFE2L2 mutations in early childhood arisen in the setting of inherited bi-allelic ABCB11 mutations</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25016225</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ABCB5</Data></Cell>
    <Cell><Data ss:Type="String">ABCB5-mediated doxorubicin transport and chemoresistance in human malignant melanoma</Data></Cell>
    <Cell><Data ss:Type="String">Our findings show that ABCB5 is a novel molecular marker for a distinct subset of chemoresistant, stem cell phenotype-expressing tumor cells among melanoma bulk populations and indicate that these chemoresistant cells can be specifically targeted via ABCB5 to enhance cytotoxic efficacy</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">15899824</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ABCB5</Data></Cell>
    <Cell><Data ss:Type="String">p-Glycoprotein ABCB5 and YB-1 expression plays a role in increased heterogeneity of breast cancer cells: correlations with cell fusion and doxorubicin resistance</Data></Cell>
    <Cell><Data ss:Type="String">Our work provides valuable insight into the drug induced cell fusion event and outcome, and suggests YB-1, GST, ABCB5 and ERK3 could be potential targets for the anti-cancer drug development against drug resistant breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">20649952</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ABCB5</Data></Cell>
    <Cell><Data ss:Type="String">Parthenolide reduces the frequency of ABCB5-positive cells and clonogenic capacity of melanoma cells from anchorage independent melanospheres</Data></Cell>
    <Cell><Data ss:Type="String">The potential clinical significance of our findings is based on the ability of parthenolide to affect both bulk and melanoma stem-like cells with clonogenic capacity and high expression of the ABCB5 transporter</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23192276</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ABCB5</Data></Cell>
    <Cell><Data ss:Type="String">△Np73 regulates the expression of the multidrug-resistance genes ABCB1 and ABCB5 in breast cancer and melanoma cells - a short report</Data></Cell>
    <Cell><Data ss:Type="String">In addition, we found that exogenous expression of △Np73 led to an increase in the expression of ABCB1 and ABCB5 in the breast cancer-derived cell lines tested, while knocking down of △Np73 resulted in a reduction in ABCB1 and ABCB5 expression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28677036</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ABCB5</Data></Cell>
    <Cell><Data ss:Type="String">ABCB5-ZEB1 Axis Promotes Invasion and Metastasis in Breast Cancer Cells</Data></Cell>
    <Cell><Data ss:Type="String">The expression of ZEB1 in tissues is positively relevant to ABCB5 in breast cancer. Knocking down ZEB1 inhibits ABCB5 ectopic expression-induced migration and invasion, as well as EMT</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28281973</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ABCC9</Data></Cell>
    <Cell><Data ss:Type="String">Gene expression of membrane transporters: Importance for prognosis and progression of ovarian carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">ABCA2, ABCA9, ABCA10, ABCC9, ABCG2 and SLC16A14 present novel putative markers of EOC progression and together with the revealed relationship between ABCA12, ABCC3, ABCC6, ABCD3, ABCG1 and SLC22A5 expression, and high grade serous type of EOC should be further examined by larger follow-up study</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26820484</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">AC092620.3</Data></Cell>
    <Cell><Data ss:Type="String">LncRNA expression profiling and its relationship with DNA damage in Cr (VI)-treated 16HBE cells</Data></Cell>
    <Cell><Data ss:Type="String">AC092620.3 were nonlinearly decreasing with the change of the DNA content of comet tails (Tail DNA), tail length (TLL), tail moment (TM) and Olive Tail Moment (OTM), and the fitting results of Tail DNA and TM were statistically significant (P?&lt;?0.05)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30476843</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ADAM10</Data></Cell>
    <Cell><Data ss:Type="String">Protease Cargo in Circulating Exosomes of Breast Cancer and Ovarian Cancer Patients</Data></Cell>
    <Cell><Data ss:Type="String">The mature ADAM10 in exosomes and its proteolytic activity is regulated by tetraspanins CD9, CD81, CD82, which was associated with breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">30678441</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ADAM10</Data></Cell>
    <Cell><Data ss:Type="String">Identification of ADAM10 as a major source of HER2 ectodomain sheddase activity in HER2 overexpressing breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">Consistent with ADAM10 being a major determinant of HER2 shedding, the inhibition of which, may provide a novel therapeutic approach for treating a variety of cancers with active HER2 signalin</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">16627989</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ADAM10</Data></Cell>
    <Cell><Data ss:Type="String">ADAM10: a new player in breast cancer progression?</Data></Cell>
    <Cell><Data ss:Type="String">ADAM10 is likely to be involved in breast cancer progression, especially in the basal subtype</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26284334</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ADAM10</Data></Cell>
    <Cell><Data ss:Type="String">Endostatin and irradiation modifies the activity of ADAM10 and neprilysin in breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">ES independently potentiates the activity of ADAM10 and NEP enzymes in 4T1 and 4THMpc breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27430992</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ADAM10</Data></Cell>
    <Cell><Data ss:Type="String">Effects of ADAM10 and ADAM17 Inhibitors on Natural Killer Cell Expansion and Antibody-dependent Cellular Cytotoxicity Against Breast Cancer Cells?In Vitro</Data></Cell>
    <Cell><Data ss:Type="String">The inhibition of ADAM17 enhanced the purity of expanded NK cells and the ADCC activity of these cells against trastuzumab treated breast cancer cell lines</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28982863</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ADAM10</Data></Cell>
    <Cell><Data ss:Type="String">Proteolytic cleavage of amyloid precursor protein by ADAM10 mediates proliferation and migration in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">ADAM10 was the key α-secretase. APP and ADAM10 co-expression was associated with worse survival in non-luminal breast cancers</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30470613</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ADAM10</Data></Cell>
    <Cell><Data ss:Type="String">Elevated serum HER-2 predicts poor prognosis in breast cancer and is correlated to ADAM10 expression</Data></Cell>
    <Cell><Data ss:Type="String">Serum HER-2 ECD could be a biomarker to identify the subgroup of poorer outcome among HER-2 overexpression breast cancer patients. Inhibition of ADAM10 activity may have potential therapeutic benefit for this most aggressive tumor subgroup</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30661303</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ADCYAP1</Data></Cell>
    <Cell><Data ss:Type="String">DcR3 protects islet beta cells from apoptosis through modulating Adcyap1 and Bank1 expression</Data></Cell>
    <Cell><Data ss:Type="String">Forced overexpression of Adcyap1 by plasmid transfection or knockdown of Bank1 expression by small interfering RNA in insulinoma NIT-1 cells protected them from cytokine-triggered apoptosis, indicating that indeed DcR3 protects beta cells via the action of these two downstream molecules</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">20007581</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ADCYAP1</Data></Cell>
    <Cell><Data ss:Type="String">The role of ADCYAP1, adenylate cyclase activating polypeptide 1, as a methylation biomarker for the early detection of cervical cancer</Data></Cell>
    <Cell><Data ss:Type="String">ADCYAP1 gene expression was reactivated by the treatment of a DNA methyltransferase inhibitor of 5'-aza-2'deoxycytidine and/or a histone deacetylase inhibitor of trichostain A in cervical cancer cells suggesting that hypermethylation in the ADCYAP1 promoter is responsible for the transcriptional silencing of the ADCYAP1 gene in cervical cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21109983</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ADCYAP1</Data></Cell>
    <Cell><Data ss:Type="String">DNA methylation in human papillomavirus-infected cervical cells is elevated in high-grade squamous intraepithelial lesions and cancer</Data></Cell>
    <Cell><Data ss:Type="String">DNA methylation status of MAL, ADCYAP1, PAX1 and CADM in 205 patients with low-grade or high-grade CIN and cervical cancer demonstrated that ADCYAP1 and PAX1 had a relatively better discriminatory ability than did methylated MAL and CADM1, which illustrates that the best panel still needs to be discovered</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26768780</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ADCYAP1</Data></Cell>
    <Cell><Data ss:Type="String">Human Papillomavirus Genotypes and Methylation of CADM1, PAX1, MAL and ADCYAP1 Genes in Epithelial Ovarian Cancer Patients</Data></Cell>
    <Cell><Data ss:Type="String">In HR-HPV infected cancers, DNA methylation may be one of the mechanisms triggering the alteration in CADM1, PAX1, MAL and ADCYAP1 gene expression levels</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28240513</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ADH1A</Data></Cell>
    <Cell><Data ss:Type="String">Genetic variation in alcohol dehydrogenase (ADH1A, ADH1B, ADH1C, ADH7) and aldehyde dehydrogenase (ALDH2), alcohol consumption and gastric cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort.</Data></Cell>
    <Cell><Data ss:Type="String">Genetic variants at ADH1 and ALDH2 loci may influence gastric cancer(GC) risk, and alcohol intake may further modify the effect of ADH1 rs1230025.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22144473</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ADH1A</Data></Cell>
    <Cell><Data ss:Type="String">Distinct prognostic values of alcohol dehydrogenase mRNA expression in pancreatic adenocarcinoma.</Data></Cell>
    <Cell><Data ss:Type="String">ADH1A, ADH5, and ADH6 expression may be potential prognostic markers of pancreatic adenocarcinoma(PAAD) and in combination have a strong interaction and better predictive value for PAAD prognosis.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28769575</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ADH1A</Data></Cell>
    <Cell><Data ss:Type="String">Distinct prognostic values of alcohol dehydrogenase mRNA expression in pancreatic adenocarcinoma.</Data></Cell>
    <Cell><Data ss:Type="String">The potential mechanism of ADH1A and ADH6 in pancreatic adenocarcinoma(PAAD) prognosis was that a high expression of ADH1A and ADH6 was involved in the P450 pathway and biological processes</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28769575</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ADH1A</Data></Cell>
    <Cell><Data ss:Type="String">Prognostic value of alcohol dehydrogenase mRNA expression in gastric cancer</Data></Cell>
    <Cell><Data ss:Type="String">ADH1A and ADH1B may be potential prognostic biomarkers of GC</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29552190</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ADRA1B</Data></Cell>
    <Cell><Data ss:Type="String">Frequent reduced expression of alpha-1B-adrenergic receptor caused by aberrant promoter methylation in gastric cancers</Data></Cell>
    <Cell><Data ss:Type="String">ADRA1B gene is an important tumour-related gene frequently involved in the development and progression of gastric cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">17242706</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ADRA1B</Data></Cell>
    <Cell><Data ss:Type="String">beta-Adrenoreceptor antagonists reduce cancer cell proliferation, invasion, and migration</Data></Cell>
    <Cell><Data ss:Type="String">The ADRA1B expression was found to be higher in MCF7 cells, which is expressed 2-fold higher than HT-29 cells and 10-fold higher than HepG2 cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25026350</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ADRA1B</Data></Cell>
    <Cell><Data ss:Type="String">The prognostic value of ADRA1 subfamily genes in gastric carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">Multivariate survival analysis revealed that low expression levels of ADRA1A (HR, 0.595; 95% CI, 0.426 0.831; adjusted P=0.002) ADRA1B (HR, 0.576; 95% CI, 0.412 0.805; adjusted P=0.001) and ADRA1D (HR, 0.559; 95% CI, 0.398 0.787; adjusted P=0.001) were associated with a favourable OS</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31452791</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ALDH9A1</Data></Cell>
    <Cell><Data ss:Type="String">Common Variation at 1q24.1 (ALDH9A1) Is a Potential Risk Factor for Renal Cancer</Data></Cell>
    <Cell><Data ss:Type="String">ALDH9A1 is implicated in RCC development, further studies are required to determine the variants that are functionally relevant</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25826619</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ALDH9A1</Data></Cell>
    <Cell><Data ss:Type="String">High Aldehyde Dehydrogenase Activity Identifies Tumor-Initiating and Metastasis-Initiating Cells in Human Prostate Cancer</Data></Cell>
    <Cell><Data ss:Type="String">Relatively high expression of certain ALDH isoforms (e.g., ALDH3A2, ALDH4A1, ALDH7A1, ALDH9A1, and ALDH18A1) in primary cultures in a comparable manner as in established human prostate cancer cell line</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">20516116</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ALDH9A1</Data></Cell>
    <Cell><Data ss:Type="String">13C-Pyruvate Imaging Reveals Alterations in Glycolysis that Precede c-Myc-Induced Tumor Formation and Regression</Data></Cell>
    <Cell><Data ss:Type="String">We also examined other alanine pathway genes whose expression was altered in the pretumor state and found that two genes,?Aldh2?and?Aldh9a1, are known to be direct MYC targets</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21723511</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ANAPC1</Data></Cell>
    <Cell><Data ss:Type="String">Methylation status of ANAPC1, CDKN2A and TP53 promoter genes in individuals with gastric cancer</Data></Cell>
    <Cell><Data ss:Type="String">ANAPC1 and TP53 methylation was probably not implicated in gastric carcinogenesis in our samples</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">18622497</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ANAPC1</Data></Cell>
    <Cell><Data ss:Type="String">A comparison between genetic portraits of normal osteoblasts and osteosarcoma cell lines</Data></Cell>
    <Cell><Data ss:Type="String">Interesting genes with elevated expression in OCLs are involved in cell cycle regulation (ANAPC1, TUBG1, NUP214) and cell proliferation (IGFBP4, FTH1). ANAPC1 regulates the metaphase-to-anaphase transition, TUBG1 is a gamma-tubulin component of microtubule organizing centers, and NUP214 encodes a protein localized to the cytoplasmic face of the nuclear pore complex required for proper cell cycle progression and nucleo-cytoplasmic transport</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19336861</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ANAPC1</Data></Cell>
    <Cell><Data ss:Type="String">A genetic variation in microRNA target site of ETS2 is associated with clinical outcomes of paclitaxel-cisplatin chemotherapy in non-small cell lung cancer</Data></Cell>
    <Cell><Data ss:Type="String">ANAPC1 rs3814026C&gt;T, ETS2 rs461155A&gt;G, SORBS1 rs7081076C&gt;A and POLR2A rs2071504C&gt;T could predict both chemotherapy response and survival</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26893365</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">APC1</Data></Cell>
    <Cell><Data ss:Type="String">SCaMC-1 Promotes Cancer Cell Survival by Desensitizing Mitochondrial Permeability Transition via ATP/ADP-mediated Matrix Ca(2+) Buffering</Data></Cell>
    <Cell><Data ss:Type="String">Knockdown of APC1 increased cancer cell sensitivity to oxidative stress-induced?apoptosis, while its overexpression protected them from death;Selective inhibition of APC1 was thus suggested to be a promising anticancer strategy </Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22015608</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ARF6</Data></Cell>
    <Cell><Data ss:Type="String">The EGFR-GEP100-Arf6-AMAP1 Signaling Pathway Specific to Breast Cancer Invasion and Metastasis</Data></Cell>
    <Cell><Data ss:Type="String">GEP100 (BRAG2) to be responsible for the Arf6 activation to induce invasion and metastasis, by directly binding to ligand-activated epidermal growth factor receptor (EGFR)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19416474</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ARF6</Data></Cell>
    <Cell><Data ss:Type="String">ARF6 promotes the formation of Rac1 and WAVE-dependent ventral F-actin rosettes in breast cancer cells in response to epidermal growth factor</Data></Cell>
    <Cell><Data ss:Type="String">A role for ARF6 in linking EGF-receptor signaling to Rac1 recruitment and activation at the plasma membrane to promote breast cancer cell directed migration</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25799492</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ARF6</Data></Cell>
    <Cell><Data ss:Type="String">Requirement for Arf6 in breast cancer invasive activities</Data></Cell>
    <Cell><Data ss:Type="String">GTP hydrolysis-defective mutant Arf6(Q67L) and the GTP-binding defective mutant Arf6(T27N) both blocked these invasive activities but not cell adhesion, suggesting the necessity of continued activation and cycling of the Arf6 GTPase cycle in invasion</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25799492</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ARF6</Data></Cell>
    <Cell><Data ss:Type="String">Roles of Arf6 in cancer cell invasion, metastasis and proliferation</Data></Cell>
    <Cell><Data ss:Type="String">The ability of tumor invasion and metastasis can be suppressed when Arf6 activity is blocked by the inhibitors or small-interfering RNAs of Arf6;the ability of tumor invasion and metastasis can be suppressed when Arf6 activity is blocked by the inhibitors or small-interfering RNAs of Arf6</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28625359</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">BARD1</Data></Cell>
    <Cell><Data ss:Type="String">BARD1, a possible biomarker for breast and ovarian cancer</Data></Cell>
    <Cell><Data ss:Type="String">A blood test based on BARD1, a protein that interacts with the breast cancer gene product BRCA1, is a promising candidate for fulfilling these conditions</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19959210</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">BARD1</Data></Cell>
    <Cell><Data ss:Type="String">Common genetic variation at BARD1 is not associated with breast cancer risk in BRCA1 or BRCA2 mutation carriers</Data></Cell>
    <Cell><Data ss:Type="String">Interactors of BRCA1/2 have been implicated as modifiers of BRCA1/2-associated cancer risk. Our finding that BARD1 does not contribute to this risk modification may focus research on other genes that do modify BRCA1/2-associated cancer risk</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21393566</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">BARD1</Data></Cell>
    <Cell><Data ss:Type="String">Cancer predisposing BARD1 mutations affect exon skipping and are associated with overexpression of specific BARD1 isoforms</Data></Cell>
    <Cell><Data ss:Type="String">Germline mutations of BARD1 may predispose to breast and/or ovarian cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26329992</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">BARD1</Data></Cell>
    <Cell><Data ss:Type="String">Dualistic Role of BARD1 in Cancer</Data></Cell>
    <Cell><Data ss:Type="String">Further evidence for a dualistic role came with the identification of BARD1 as a neuroblastoma predisposition gene in our genome wide association study which has demonstrated that single nucleotide polymorphisms in BARD1 can correlate with risk or can protect against cancer based on their association with the expression of FL and splice variants of BARD1</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29292755</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">BARD1</Data></Cell>
    <Cell><Data ss:Type="String">BARD1 is A Low/Moderate Breast Cancer Risk Gene: Evidence Based on An Association Study of the Central European p.Q564X Recurrent Mutation</Data></Cell>
    <Cell><Data ss:Type="String">Substantial evidence for the association of a deleterious BARD1 mutation with BC as a low/moderate risk allele</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31142030</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">BDKRB2</Data></Cell>
    <Cell><Data ss:Type="String">Mitogenic signalling by B2 bradykinin receptor in epithelial breast cells</Data></Cell>
    <Cell><Data ss:Type="String">The bradykininin receptor B2 (BDKRB2) gene is known to induce mitosis in breast cells and enhance progression of cancer.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">15281091</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">BDKRB2</Data></Cell>
    <Cell><Data ss:Type="String">Bradykinin stimulates cell proliferation through an extracellular-regulated kinase 1 and 2-dependent mechanism in breast cancer cells in primary culture</Data></Cell>
    <Cell><Data ss:Type="String">The mitogenic effects of BK are retained in peritumour and tumour cells; hence, it is likely that BK has an important role in cancer endorsement and progression.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">16079255</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">BDKRB2</Data></Cell>
    <Cell><Data ss:Type="String">Cytogenetic and cDNA microarray expression analysis of MCF10 human breast cancer progression cell lines</Data></Cell>
    <Cell><Data ss:Type="String">Tissue kallikrein was found in malignant human breast tissue and bradykinin (BK) stimulates the proliferation of immortalised breast cancer cells.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19584277</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">BDKRB2</Data></Cell>
    <Cell><Data ss:Type="String">CLOCK in breast tumorigenesis: genetic, epigenetic, and transcriptional profiling analyses</Data></Cell>
    <Cell><Data ss:Type="String">BDKRB2 (2.1-fold decrease, Q = 1.63 E 3), which induces proliferation in human epithelial breast cells.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">20124474</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">BID</Data></Cell>
    <Cell><Data ss:Type="String">Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis</Data></Cell>
    <Cell><Data ss:Type="String">We report here that BID, a BH3 domain-containing proapoptotic Bcl2 family member, is a specific proximal substrate of Casp8 in the Fas apoptotic signaling pathway</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">9727492</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">BID</Data></Cell>
    <Cell><Data ss:Type="String">BID-deficient breast cancer MCF-7 cells as a model for the study of autophagy in cancer therapy</Data></Cell>
    <Cell><Data ss:Type="String">BID(+) and BID(-) breast cancer MCF-7 cells could be considered to be a useful model for the study of the molecular interdependences between apoptosis and autophagy and the role of both processes in cancer therapy.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">16874058</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">BID</Data></Cell>
    <Cell><Data ss:Type="String">Controlled delivery of BID protein fused with TAT peptide sensitizes cancer cells to apoptosis</Data></Cell>
    <Cell><Data ss:Type="String">TAT-BID may be delivered to cancer cells in controlled manner and efficiently sensitizes PC3 and A549 cells to TRAIL</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25326334</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">BID</Data></Cell>
    <Cell><Data ss:Type="String">Synergy of BID with doxorubicin in the killing of cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">TAT-BID and doxorubicin may thus be considered as a potential therapeutic combination for cervical carcinoma and advanced prostate cancer treatment</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25760094</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">BIRC5</Data></Cell>
    <Cell><Data ss:Type="String">Early diagnostic value of survivin and its alternative splice variants in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Differential expression of exosomal-Survivin, particularly Survivin-2B, may serve as a diagnostic and/or prognostic marker</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">24620748</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">BIRC5</Data></Cell>
    <Cell><Data ss:Type="String">The expression of BIRC5 is correlated with loss of specific chromosomal regions in breast carcinomas.</Data></Cell>
    <Cell><Data ss:Type="String">BIRC5 expression may induce breast tumor proliferation by promoting genetic instability. </Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">18181175</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">BIRC5</Data></Cell>
    <Cell><Data ss:Type="String">BIRC5 Genomic Copy Number Variation in Early-Onset Breast Cancer</Data></Cell>
    <Cell><Data ss:Type="String">BIRC5 gene has the potential to be a marker for the detection and prognosis of cancer at an early age.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27372966</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">BIRC5</Data></Cell>
    <Cell><Data ss:Type="String">BIRC5 (survivin): a pejorative prognostic marker in stage II/III breast cancer with no response to neoadjuvant chemotherapy.</Data></Cell>
    <Cell><Data ss:Type="String">BIRC5 (survivin) as a main pejorative prognostic factor in patients with breast cancers with no pCR.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27592112</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">BIRC5</Data></Cell>
    <Cell><Data ss:Type="String">Downregulation of BIRC5 inhibits the migration and invasion of esophageal cancer cells by interacting with the PI3K/Akt signaling pathway</Data></Cell>
    <Cell><Data ss:Type="String">BIRC5 is able to inhibit the migration and invasion of tumor cells, and regulate the expression of angiogenesis?associated factors.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30127937</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">BLZF1</Data></Cell>
    <Cell><Data ss:Type="String">A Role for the Nucleosome Assembly Proteins TAF-Iβ and NAP1 in the Activation of BZLF1 Expression and Epstein-Barr Virus Reactivation</Data></Cell>
    <Cell><Data ss:Type="String">Quantification of the percentage of BLZF1-expressing cells showed that, like TAF-Iβ, NAP1 overexpression can induce BZLF1 expression, whereas TAF-Iα overexpression did not induce BZLF1 expression, despite being expressed at a higher level than TAF-Iβ</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23691099</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">BLZF1</Data></Cell>
    <Cell><Data ss:Type="String">BLZF1 expression is of prognostic significance in hepatocellular carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">BLZF1 is a novel unfavorable biomarker for prognosis of patients with HCC</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26342799</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">BLZF1</Data></Cell>
    <Cell><Data ss:Type="String">BLZF1 expression is of prognostic significance in hepatocellular carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">The prognostic value of BLZF1 was further confirmed by stratified analyses</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26342799</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CACNB2</Data></Cell>
    <Cell><Data ss:Type="String">Randomness and preserved patterns in cancer network</Data></Cell>
    <Cell><Data ss:Type="String">CACNB2 was downregulated in breast cancer cells, thereby causing poor signaling by negatively affecting the calcium metabolism</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25220184</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CASC3</Data></Cell>
    <Cell><Data ss:Type="String">Genomic analysis of the HER2/TOP2A amplicon in breast cancer and breast cancer cell lines</Data></Cell>
    <Cell><Data ss:Type="String">The amplification of the HER2/TOP2A region has been correlated with the overexpression of several additional genes, such as CASC3, CDC6, RARA, and?SMARCE1</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">18332872</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CASC3</Data></Cell>
    <Cell><Data ss:Type="String">Identification of Novel Breast Cancer Subtype-Specific Biomarkers by Integrating Genomics Analysis of DNA Copy Number Aberrations and miRNA-mRNA Dual Expression Profiling</Data></Cell>
    <Cell><Data ss:Type="String">?In the luminal-A loss related Bayesian network motif, BRCA1 showed the most links with other biomarkers, including two miRNAs (miR-143 and miR-145) and 4 genes (CASC3, ITGA2B, BID, and LMNB1)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25961039</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CASC3</Data></Cell>
    <Cell><Data ss:Type="String">Methylation-regulated miR-124-1 suppresses tumorigenesis in hepatocellular carcinoma by targeting CASC3</Data></Cell>
    <Cell><Data ss:Type="String">MiR-124-1-mediated downregulation of CASC3 resulted in the inactivation of p38-MAPK, JNK and ERK</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27029030</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CASP7</Data></Cell>
    <Cell><Data ss:Type="String">IFNgamma restores breast cancer sensitivity to fulvestrant by regulating STAT1, IFN regulatory factor 1, NF-kappaB, BCL2 family members, and signaling to caspase-dependent apoptosis</Data></Cell>
    <Cell><Data ss:Type="String">This molecular signaling is associated with the activation of signal transducer and activator of transcription 1 and leads to increased mitochondrial membrane permeability; activation of caspase-7 (CASP7), CASP8, and CASP9; and induction of apoptosis but not autophagy. Whereas antiestrogen-resistant cells are capable of inducing autophagy through IFN-mediated signaling, their ability to do so through antiestrogen-regulated signaling is lost</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">20457620</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CASP7</Data></Cell>
    <Cell><Data ss:Type="String">Influence of DNA copy number and mRNA levels on the expression of breast cancer related proteins</Data></Cell>
    <Cell><Data ss:Type="String">Such pattern might be an indication of hsa-miR-29c miRNA functioning as a repressor of translation of CASP7 within the luminal-A subtype</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23562353</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CASP7</Data></Cell>
    <Cell><Data ss:Type="String">Targeting the XIAP/caspase-7 complex selectively kills caspase-3-deficient malignancies</Data></Cell>
    <Cell><Data ss:Type="String">CASP3/DR combined with p19/p12-CASP7 accumulation correlated with the aggressive evolution of clinical malignancies and a poor prognosis in cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23979166</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CASP7</Data></Cell>
    <Cell><Data ss:Type="String">Overexpression of caspase 7 is ERα dependent to affect proliferation and cell growth in breast cancer cells by targeting p21(Cip)</Data></Cell>
    <Cell><Data ss:Type="String">CASP7 is aberrantly expressed in breast cancer and contributes to cell growth and proliferation by downregulating p21(Cip) protein, suggesting that targeting CASP7-positive breast cancer could be one of the potential therapeutic strategies</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27089142</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CASP7</Data></Cell>
    <Cell><Data ss:Type="String">Low cleaved caspase-7 levels indicate unfavourable outcome across all breast cancers</Data></Cell>
    <Cell><Data ss:Type="String">BCL2 levels are elevated in breast cancer where they are marker of good prognosis. BCL2 and active caspase levels correlate negatively; yet, active caspases indicate good outcome. Low BCL2 and low caspase-7 are highly prognostic of unfavourable outcome across all breast cancers. BCL2 levels indicate molecular subtype and tumour proliferation status in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30069746</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CCKBR</Data></Cell>
    <Cell><Data ss:Type="String">A single nucleotide polymorphism of the cholecystokinin-B receptor predicts risk for pancreatic cancer</Data></Cell>
    <Cell><Data ss:Type="String">Single nucleotide polymorphism (SNP) in the cholecystokinin B receptor (CCKBR) gene predicts survival and risk of pancreatic cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22277584</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CCKBR</Data></Cell>
    <Cell><Data ss:Type="String">A single nucleotide polymorphism of the cholecystokinin-B receptor predicts risk for pancreatic cancer</Data></Cell>
    <Cell><Data ss:Type="String">Growth of human pancreatic cancer is stimulated by gastrin through the CCKBR and an alternatively spliced isoform of the CCKBR gene called CCKCR</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22277584</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CCKBR</Data></Cell>
    <Cell><Data ss:Type="String">MiR-148a regulates the growth and apoptosis in pancreatic cancer by targeting CCKBR and Bcl-2</Data></Cell>
    <Cell><Data ss:Type="String">MiR-148a's targeting of CCKBR and Bcl-2 in the regulation of pancreatic cancer growth and apoptosis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23975374</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CCKBR</Data></Cell>
    <Cell><Data ss:Type="String">Heterogeneous expression of cholecystokinin and gastrin receptor in stomach and pancreatic cancer: An immunohistochemical study</Data></Cell>
    <Cell><Data ss:Type="String">Significantly higher expression of CCKAR and down regulation of CCKBR in PC as compared to control while CCKBR/GR was detected in majority of SC samples</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27072272</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CCKBR</Data></Cell>
    <Cell><Data ss:Type="String">Expression of the Cholecystokinin-B Receptor in Neoplastic Gastric Cells</Data></Cell>
    <Cell><Data ss:Type="String">All eight NENs expressed CCKBR and neuroendocrine markers in a majority of tumor cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28980157</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CCKBR</Data></Cell>
    <Cell><Data ss:Type="String">Low serum gastrin associated with ER+ breast cancer development via inactivation of CCKBR/ERK/P65 signaling</Data></Cell>
    <Cell><Data ss:Type="String">CCKBR/ERK/P65 signaling function is generally tumor suppressive in ER+ BC, indicating therapies should focus on restoring, not inhibiting, CCKBR/ERK/P65 pathway activity</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30115027</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CD24</Data></Cell>
    <Cell><Data ss:Type="String">Loss of EpCAM expression in breast cancer derived serum exosomes: Role of proteolytic cleavage</Data></Cell>
    <Cell><Data ss:Type="String">We suggest that CD24 could be an additional marker for the enrichment of tumor-derived exosomes from blood</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">21601258</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CD24</Data></Cell>
    <Cell><Data ss:Type="String">CD24 expression is a new prognostic marker in breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">CD24 expression in primary breast cancer as detected by immunohistochemistry might be a new marker for a more aggressive breast cancer biology.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">14581365</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CD24</Data></Cell>
    <Cell><Data ss:Type="String">CD24 Overexpression Is Associated with Poor Prognosis in Luminal A and Triple-Negative Breast Cancer.</Data></Cell>
    <Cell><Data ss:Type="String">CD24 overexpression is an independent unfavourable prognostic factor in breast cancer, especially for luminal A and TNBC subtypes, and CD24 may be a promising therapeutic target for specific subtypes of breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26444008</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CD24</Data></Cell>
    <Cell><Data ss:Type="String">CD24 Overexpression Is Associated with Poor Prognosis in Luminal A and Triple-Negative Breast Cancer.</Data></Cell>
    <Cell><Data ss:Type="String">CD24 gene expression was associated with histone acetylation independent of DNA methylation, suggesting its epigenetic regulation in breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26444008</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CD24</Data></Cell>
    <Cell><Data ss:Type="String">Prognostic significance of CD24 and CD44 in breast cancer: a meta-analysis.</Data></Cell>
    <Cell><Data ss:Type="String">CD24 may play a role in tumorigenesis and cancer progression.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27470135</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CD24</Data></Cell>
    <Cell><Data ss:Type="String">CD24 is a Potential Biomarker for Prognosis in Human Breast Carcinoma.</Data></Cell>
    <Cell><Data ss:Type="String">CD24 and SDC1 can serve as prognostic indicators for breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30001552</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CD47</Data></Cell>
    <Cell><Data ss:Type="String">A rapid,automated surface protein profiling of single circulating exosomes in human blood</Data></Cell>
    <Cell><Data ss:Type="String">A differential CD47 expression in blood-derived individual circulating exosomes that is correlated with breast cancer status, demonstrating a great potential of individual exosome profiles in biomarker discovery</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">27819324</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CD47</Data></Cell>
    <Cell><Data ss:Type="String">HIF-1 regulates CD47 expression in breast cancer cells to promote evasion of phagocytosis and maintenance of cancer stem cells</Data></Cell>
    <Cell><Data ss:Type="String">High CD47 expression is correlated with increased HIF target gene expression and decreased patient survival.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26512116</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CD47</Data></Cell>
    <Cell><Data ss:Type="String">HIF-1 regulates CD47 expression in breast cancer cells to promote evasion of phagocytosis and maintenance of cancer stem cells</Data></Cell>
    <Cell><Data ss:Type="String">CD47 expression contributes to the lethal breast cancer phenotype that is mediated by HIF-1.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26512116</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CD47</Data></Cell>
    <Cell><Data ss:Type="String">Significance of CD47 expression in gastric cancer.</Data></Cell>
    <Cell><Data ss:Type="String">Low expression of CD47 was associated with the advancement of gastric cancer, in contrast to other cancers, and it may be associated with a decrease in lymphocytes during later stages.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28693236</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CD47</Data></Cell>
    <Cell><Data ss:Type="String">Combined high expression of CD47 and CD68 is a novel prognostic factor for breast cancer patients.</Data></Cell>
    <Cell><Data ss:Type="String">Combined detection of CD47 and CD68 may provide guidance for the prognosis of breast cancer, especially hormone receptor-negative breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31528120</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CD47</Data></Cell>
    <Cell><Data ss:Type="String">Prognostic significance of CD47 in human malignancies: a systematic review and meta-analysis</Data></Cell>
    <Cell><Data ss:Type="String">CD47 could be a useful prognostic indicator in cancer patients and may be a useful therapeutic target.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CD47</Data></Cell>
    <Cell><Data ss:Type="String">Role of the expression of PD-L1 and CD47 on circulating tumor cells (CTCs) in the prediction of outcome in metastatic breast cancer (mBC) patients.</Data></Cell>
    <Cell><Data ss:Type="String">The detection of high CD47 and/or PD-L1 expression on CTCs is associated with triple-negative tumors, disease progression and poor patient outcome and could serve for the refinement of prognosis in mBC.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CD82</Data></Cell>
    <Cell><Data ss:Type="String">Exosomal protein CD82 as a diagnostic biomarker for precision medicine for breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">CD82 expression in exosomes from breast cancer samples is a sensitive biomarker</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">30604894</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CD82</Data></Cell>
    <Cell><Data ss:Type="String">Correlation of reduction in MRP-1/CD9 and KAI1/CD82 expression with recurrences in breast cancer patients.</Data></Cell>
    <Cell><Data ss:Type="String">The expression of MRP-1/CD9 and KAI1/CD82genes are useful indicators of a poor prognosis in breast cancer patients.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">9736046</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CD82</Data></Cell>
    <Cell><Data ss:Type="String">Prognostic significance of KAI1/CD82 in human melanoma and its role in cell migration and invasion through the regulation of ING4.</Data></Cell>
    <Cell><Data ss:Type="String">KAI1 may be used as a promising prognostic marker and a possible therapeutic target for human melanoma.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24130172</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CD82</Data></Cell>
    <Cell><Data ss:Type="String">Prognostic significance of KAI1/CD82 in human melanoma and its role in cell migration and invasion through the regulation of ING4.</Data></Cell>
    <Cell><Data ss:Type="String">Overexpression of KAI1 significantly inhibited melanoma cell migration through suppression of Rho-associated kinase-mediated formation of stress fiber.overexpression of KAI1 significantly inhibited melanoma cell invasion by reducing the activity of metalloproteinase-2.melanoma cell migration by KAI1 is mediated by another tumor-suppressor protein called inhibitor of growth 4 through the regulation of p65.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24130172</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CD82</Data></Cell>
    <Cell><Data ss:Type="String">Effect and prognostic significance of the KAI1 gene in human gastric carcinoma.</Data></Cell>
    <Cell><Data ss:Type="String">The expression of KAI1 protein and mRNA was associated with the differentiation degree of gastric cancer, presence of lymph node metastasis, tumor-node-metastasis stage, depth of invasion and the survival time of patients.Patients that expressed KAI1 may demonstrate an improved prognosis.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26622792</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CD82</Data></Cell>
    <Cell><Data ss:Type="String">Effect and prognostic significance of the KAI1 gene in human gastric carcinoma.</Data></Cell>
    <Cell><Data ss:Type="String">The tumor suppressor gene KAI1 inhibits the migration and invasion of gastric carcinoma cells, possibly by suppressing the expression of uPA.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26622792</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CD82</Data></Cell>
    <Cell><Data ss:Type="String">Prognostic role of CD82/KAI1 in multiple human malignant neoplasms: a meta-analysis of 31 studies</Data></Cell>
    <Cell><Data ss:Type="String">CD82 could be a promising biomarker for predicting the prognosis of patients with malignant neoplasms, and the biological functions of CD82 are of great research value of the subject.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29263677</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CD82</Data></Cell>
    <Cell><Data ss:Type="String">Exosomal protein CD82 as a diagnostic biomarker for precision medicine for breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">CD82 expression in breast cancer tissue was significantly lower than that in healthy and benign breast disease tissues. There was a significant negative correlation between CD82 expression in tissues and CD82 content in exosomes, which indicated that CD82 expression was redistributed from tissues to the blood with the development and metastasis of breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30604894</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CDC23</Data></Cell>
    <Cell><Data ss:Type="String">CDC23 regulates cancer cell phenotype and is overexpressed in papillary thyroid cancer</Data></Cell>
    <Cell><Data ss:Type="String">CDC23 is a critical regulator of cell cycle and cell growth, and may be involved in thyroid cancer initiation and progression, and may explain the different tumor biology observed by gender</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21990323</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CDC23</Data></Cell>
    <Cell><Data ss:Type="String">Expression of miR-34c induces G2/M cell cycle arrest in breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">The levels of CDC23, an important mediator in mitotic progression, were suppressed following miR-34c expression, and siRNAs targeting CDC23 mimicked the effect of miR-34c on G2/M arrest</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25064703</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CDC23</Data></Cell>
    <Cell><Data ss:Type="String">Low-dose staurosporine selectively reverses BCR-ABL-independent IM resistance through PKC-α-mediated G2/M phase arrest in chronic myeloid leukaemia</Data></Cell>
    <Cell><Data ss:Type="String">The PKC-α-dependent G2/M phase arrest was induced by down-regulation of CDC23, an important regulator of mitotic progression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30618318</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CDC42</Data></Cell>
    <Cell><Data ss:Type="String">Proteomic Profiling of Exosomes Secreted by Breast Cancer Cells with Varying Metastatic Potential</Data></Cell>
    <Cell><Data ss:Type="String">Presumably aid in targeting the primary cancer cells to specific metastatic sites</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29115712</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CDC42</Data></Cell>
    <Cell><Data ss:Type="String">Role of Activated Rac1/Cdc42 in Mediating Endothelial Cell Proliferation and Tumor Angiogenesis in Breast Cancer</Data></Cell>
    <Cell><Data ss:Type="String">Rac1/Cdc42 is a vascular regulator of tumor angiogenesis and that it may reduce stability of the p53 protein to promote VEGF expression by enhancing p53 protein ubiquitin.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23750283</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CDC42</Data></Cell>
    <Cell><Data ss:Type="String">Cdc42 overexpression induces hyperbranching in the developing mammary gland by enhancing cell migration</Data></Cell>
    <Cell><Data ss:Type="String">Cdc42 overexpression disrupts mammary gland branching morphogenesis by altering Rho GTPase and MAPK signaling, leading to increased MEC contractility and migration in association with stromal alterations</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24074261</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CDC42</Data></Cell>
    <Cell><Data ss:Type="String">Role of p-21-activated kinases in cancer progression</Data></Cell>
    <Cell><Data ss:Type="String">PAK1, MLC, ERK1/2 and Cyclin D1 are the downstream effectors of Cdc42. The expression of the PAKs can be seen in all sorts of tissues and plays an essential role in promoting tumorigenesis in various human neoplasms including breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24529727</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CDC42</Data></Cell>
    <Cell><Data ss:Type="String">Silencing of CDC42 inhibits neuroblastoma cell proliferation and transformation</Data></Cell>
    <Cell><Data ss:Type="String">CdcC42 induces invasiveness and metastatic activity by breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25264923</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CDC42</Data></Cell>
    <Cell><Data ss:Type="String">MALAT1 induced migration and invasion of human breast cancer cells by competitively binding miR-1 with cdc42</Data></Cell>
    <Cell><Data ss:Type="String">MALAT1 influenced the expression of Cdc42 by binding miR-1 competitively. There were ceRNA networks that co-regulated cell migration and invasion in breast cancer patients by MALALT1, miR-1 and Cdc42of the PAKs can be seen in all sorts of tissues and plays an essential role in promoting tumorigenesis in various human neoplasms including?breast cancer?</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26926567</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CHEK2</Data></Cell>
    <Cell><Data ss:Type="String">Cancer risks in first-degree relatives of CHEK2 mutation carriers: effects of mutation type and cancer site in proband</Data></Cell>
    <Cell><Data ss:Type="String">The risk of cancer in a carrier of a CHEK2 mutation is dependent on the family history of cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19401704</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CHEK2</Data></Cell>
    <Cell><Data ss:Type="String">Risk of breast cancer in women with a CHEK2 mutation with and without a family history of breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Women with a truncating mutation in CHEK2 and a positive family history of breast cancer have a lifetime risk of breast cancer of greater than 25% and are candidates for magnetic resonance imaging screening and for tamoxifen chemoprevention</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21876083</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CHEK2</Data></Cell>
    <Cell><Data ss:Type="String">CHEK2 contribution to hereditary breast cancer in non-BRCAfamilies</Data></Cell>
    <Cell><Data ss:Type="String">CHEK2 alleles make an appreciable contribution to breast cancer susceptibility, and their identification could help in the clinical management of patients carrying a?CHEK2?mutation</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22114986</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CHEK2</Data></Cell>
    <Cell><Data ss:Type="String">Genomic Biomarkers for Breast Cancer Risk</Data></Cell>
    <Cell><Data ss:Type="String">Genomic biomarkers for breast cancer are comprised of rare highly penetrant mutations of genes such as BRCA1 or BRCA2, moderately penetrant mutations of genes such as?CHEK2, as well as more common genomic variants, including single nucleotide polymorphisms, associated with modest effect sizes</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26987529</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CHEK2</Data></Cell>
    <Cell><Data ss:Type="String">Prognostic Significance of CHEK2 Mutation in Progression of Breast Cancer</Data></Cell>
    <Cell><Data ss:Type="String">Detection of mutations in CHEK2 can be used as a prognostic factor for patient response to treatment and for targeting downstream molecules of CHEK2 that are involved in the proliferation of breast tumor cells</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31220302</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CP</Data></Cell>
    <Cell><Data ss:Type="String">Proteomic Profiling of Exosomes Secreted by Breast Cancer Cells with Varying Metastatic Potential</Data></Cell>
    <Cell><Data ss:Type="String">Presumably aid in targeting the primary cancer cells to specific metastatic sites</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29115712</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CP</Data></Cell>
    <Cell><Data ss:Type="String">Evidence for increased non-ceruloplasmin copper in early-stage human breast cancer serum</Data></Cell>
    <Cell><Data ss:Type="String">This high serum copper-to-ceruloplasmin ratio in BC patients may reflect disordered copper metabolism in this disease, which could also have implications for the origin of, or the response to, the cancer proces</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">1584712</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CP</Data></Cell>
    <Cell><Data ss:Type="String">Use of ceruloplasmin levels to monitor response to therapy and predict recurrence of breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">In following patients with breast cancer, we noted that in those patients that recurred, the CP level became elevated 16-34 weeks prior to any clinical evidence of metastases</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">6616078</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CP</Data></Cell>
    <Cell><Data ss:Type="String">Copper and ceruloplasmin levels in serum of women with breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Levels copper and ceruloplasmin may help in prognosis &amp; diagnosis of disease</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">9808908</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CP</Data></Cell>
    <Cell><Data ss:Type="String">Searching for early breast cancer biomarkers by serum protein profiling of pre-diagnostic serum; a nested case-control study</Data></Cell>
    <Cell><Data ss:Type="String">With 2D-nanoLC-MS/MS, afamin, apolipoprotein E and isoform 1 of inter-alpha trypsin inhibitor heavy chain H4 (ITIH4) were found to be higher in pre-diagnostic breast cancer (p &lt; 0.05), while alpha-2-macroglobulin and ceruloplasmin were lower (p &lt; 0.05</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21871081</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CP</Data></Cell>
    <Cell><Data ss:Type="String">The relationship between serum level of copper and ceruloplasmin and pathologic and clinical characteristics in early breast cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">Copper and ceruloplasmin might also play an important role in early procedure of breast cancer, and need collect more data in the future to validate</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CSTB</Data></Cell>
    <Cell><Data ss:Type="String">Identification of Cystatin B as a Potential Serum Marker in Hepatocellular Carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">CSTB or the combination of CSTB and alpha-fetoprotein may be a useful marker for diagnosing patients with HCC with a high sensitivity</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">18281540</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CSTB</Data></Cell>
    <Cell><Data ss:Type="String">Identification of Cystatin B as a Potential Serum Marker in Hepatocellular Carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">CSTB is specifically overexpressed in most HCCs and is also elevated in the serum of a large proportion of HCC patients</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">18281540</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CSTB</Data></Cell>
    <Cell><Data ss:Type="String">Cystatin B is a progression marker of human epithelial ovarian tumors mediated by the TGF-β signaling pathway</Data></Cell>
    <Cell><Data ss:Type="String">CSTB may become a novel diagnostic intracellular biomarker for the early detection of ovarian cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24452274</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CSTB</Data></Cell>
    <Cell><Data ss:Type="String">Cystatin B is a progression marker of human epithelial ovarian tumors mediated by the TGF-β signaling pathway</Data></Cell>
    <Cell><Data ss:Type="String">The increased CSTB expression in ovarian tissue represents tumor progression and is dysregulated by the TGF-β signaling pathway.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24452274</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CSTB</Data></Cell>
    <Cell><Data ss:Type="String">Expression and epigenetic regulation of cystatin B in lung cancer and colorectal cancer</Data></Cell>
    <Cell><Data ss:Type="String">CSTB might be a potential prognostic marker for patients with primary lung cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29037838</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CSTB</Data></Cell>
    <Cell><Data ss:Type="String">Expression and epigenetic regulation of cystatin B in lung cancer and colorectal cancer</Data></Cell>
    <Cell><Data ss:Type="String">In colorectal tumors, CSTB was not linked to any clinicopathological parameters including age, size of tumor, lymph node metastasis and tumor grading</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29037838</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CSTB</Data></Cell>
    <Cell><Data ss:Type="String">Combining discovery and targeted proteomics reveals a prognostic signature in oral cancer</Data></Cell>
    <Cell><Data ss:Type="String">Assessing the protein profiles of large and small neoplastic islands and their surrounding stroma by combining laser microdissection (LMD) and proteomics reveals several proteins-including CSTB, NDRG1, LTA4H, PGK1, COL6A1, ITGAV, and MB-ith distinct expression patterns between ITF and inner tumor, suggesting a potential prognostic value by clinicopathological association analysis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30185791</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CTSB</Data></Cell>
    <Cell><Data ss:Type="String">Cathepsin B: a potential prognostic marker for inflammatory breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">CTSB may initiate proteolytic pathways crucial for IBC invasion. Thus, our data demonstrate that CTSB may be a potential prognostic marker for lymph node metastasis in IBC</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21199580</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CTSB</Data></Cell>
    <Cell><Data ss:Type="String">Hormonal-receptor positive breast cancer: IL-6 augments invasion and lymph node metastasis via stimulating cathepsin B expression</Data></Cell>
    <Cell><Data ss:Type="String">IL-6-induced CTSB may play a role in lymph node metastasis, and that may possess future therapeutic implications for HRP-breast cancer patients with pLNs</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27482469</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CTSB</Data></Cell>
    <Cell><Data ss:Type="String">TRAIL DR5-CTSB crosstalk participates in breast cancer autophagy initiated by SAHA</Data></Cell>
    <Cell><Data ss:Type="String">SAHA may stimulate TRAIL DR5-CTSB crosstalk, influence the activity of downstream TOR signalling pathway mainly through the AKTs pathway, and initiate the autophagy of breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29018571</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CTSB</Data></Cell>
    <Cell><Data ss:Type="String">Proteomic analysis of lung metastases in a murine breast cancer model reveals divergent influence of CTSB and CTSL overexpression</Data></Cell>
    <Cell><Data ss:Type="String">TgCTSB and tgCTSL both display a strong and distinct impact on proteome composition of lung macrometastases in the PyMT model</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29187882</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CTSB</Data></Cell>
    <Cell><Data ss:Type="String">Synergistic antitumor effects of combined cathepsin B and cathepsin Z deficiencies on breast cancer progression and metastasis in mice</Data></Cell>
    <Cell><Data ss:Type="String">Double deficiency of Ctsb and Ctsz exerts significant synergistic anticancer effects, whereas the single deficiencies demonstrate at least partial reciprocal compensation</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">20133781</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CTSB</Data></Cell>
    <Cell><Data ss:Type="String">ErbB2-Driven Breast Cancer Cell Invasion Depends on a Complex Signaling Network Activating Myeloid Zinc Finger-1-Dependent Cathepsin B Expression</Data></Cell>
    <Cell><Data ss:Type="String">The identified signaling network activates the transcription of cathepsin B gene (CTSB) via myeloid zinc finger-1 transcription factor that binds to an ErbB2-responsive enhancer element in the first?intron?of?CTSB</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22464443</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CUL4A</Data></Cell>
    <Cell><Data ss:Type="String">A functional link between Wnt signaling and SKP2-independent p27 turnover in mammary tumors</Data></Cell>
    <Cell><Data ss:Type="String">CUL4A and CUL4B are therefore components of a conserved Wnt-induced proteasome targeting (WIPT) complex that regulates p27KIP1 levels and cell cycle progression in mammalian cells.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19056892</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CUL4A</Data></Cell>
    <Cell><Data ss:Type="String">Analysis of DNA Repair-related Genes in Breast Cancer Reveals CUL4A Ubiquitin Ligase as a Novel Biomarker of Trabectedin Response</Data></Cell>
    <Cell><Data ss:Type="String">Our observations support the notion of greater trabectedin activity in tumors exhibiting BRCAness and reveal CUL4A as a potential biomarker for definition of trabectedin target patients</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23364677</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CUL4A</Data></Cell>
    <Cell><Data ss:Type="String">CUL4A?contributes to the biology of basal-like breast tumors through modulation of cell growth and antitumor immune response</Data></Cell>
    <Cell><Data ss:Type="String">In particular, we report a putative role of CUL4A in bypassing the immune system in breast cancer through the down-regulation of several molecules involved in the immune surveillance. These findings provide insight into the oncogenic properties of CUL4A in basal-like breast cancer and highlight the therapeutic opportunities to target CUL4A</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24870930</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CUL4A</Data></Cell>
    <Cell><Data ss:Type="String">Dysregulation of CUL4A and CUL4B Ubiquitin Ligases in Lung Cancer</Data></Cell>
    <Cell><Data ss:Type="String">CUL4A and CUL4B are differentially associated with etiologic factors for pulmonary malignancies and are independent prognostic markers for the survival of distinct lung cancer subtypes</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27974468</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CUL4A</Data></Cell>
    <Cell><Data ss:Type="String">CUL4A overexpression as an independent adverse prognosticator in intrahepatic cholangiocarcinoma</Data></Cell>
    <Cell><Data ss:Type="String">Overexpression of CUL4A plays an oncogenic role in iCCA and adversely affects disease-free survival. Thus, it may prove to be a powerful prognostic factor and a potential therapeutic target</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28576144</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CUL4A</Data></Cell>
    <Cell><Data ss:Type="String">miR-377 targets CUL4A and regulates metastatic capability in ovarian cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-377 is a significant negative regulator of CUL4A that controls cancer cell progression in ovarian cancer cell lines</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29512715</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CXCL13</Data></Cell>
    <Cell><Data ss:Type="String">Chemokine CXCL13 is overexpressed in the tumour tissue and in the peripheral blood of breast cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">CXCL13 is overexpressed within breast cancer tissues, and increased serum levels of this cytokine can be found in breast cancer patients with metastatic disease pointing to a role of CXCL13 in the progression of breast cancer, suggesting that CXCL13 might serve as a useful therapeutic target and/or diagnostic marker in this malignancy</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">18781150</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CXCL13</Data></Cell>
    <Cell><Data ss:Type="String">Chemokine CXCL13 is overexpressed in the tumour tissue and in the peripheral blood of breast cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">CXCL13 is overexpressed within breast cancer tissues at the mRNA and protein levels and that increased serum levels of this cytokine can be found in breast cancer patients.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">18781150</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CXCL13</Data></Cell>
    <Cell><Data ss:Type="String">Improved outcome of high-risk early HER2 positive breast cancer with high CXCL13-CXCR5 messenger RNA expression</Data></Cell>
    <Cell><Data ss:Type="String">CXCL13-CXCR5 axis with classic determinants of poor prognosis, such as high grade, hormone receptor negativity, and axillary node involvement.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22607768</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CXCL13</Data></Cell>
    <Cell><Data ss:Type="String">Improved outcome of high-risk early HER2 positive breast cancer with high CXCL13-CXCR5 messenger RNA expression</Data></Cell>
    <Cell><Data ss:Type="String">CXCL13  were found to be negatively associated with estrogen receptor and microtubule-associated protein tau mRNA expression and with dense lymphocytic infiltration, and were positively associated with nuclear grade. CXCL13 was positively associated with HER2. Multivariate analysis revealed an association between high CXCL13 mRNA expression and improved DFS (hazard ratio [HR] 0.48 [95% CI, 0.25-0.90]; Wald, P = .023) but not OS; In the HER2 mRNA overexpressing subgroup, high CXCL13 mRNA expression was associated with improved DFS (P &lt; .001).</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22607768</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CXCL13</Data></Cell>
    <Cell><Data ss:Type="String">CXCL13-CXCR5 co-expression regulates epithelial to mesenchymal transition of breast cancer cells during lymph node metastasis</Data></Cell>
    <Cell><Data ss:Type="String">The EMT-inducing potential of CXCL13 as well as demonstrated the prognostic value of CXCL13-CXCR5 co-expression in primary BC. Moreover, CXCL13-CXCR5-RANKL-Src axis may present a therapeutic target in LNM positive BC patients</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24337540</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CXCL13</Data></Cell>
    <Cell><Data ss:Type="String">CXCL13-CXCR5 co-expression regulates epithelial to mesenchymal transition of breast cancer cells during lymph node metastasis</Data></Cell>
    <Cell><Data ss:Type="String">In CXCL13-stimulated BC cells, expression of various mesenchymal markers (Vimentin, N-cadherin), EMT regulators (Snail, Slug), and matrix metalloproteinase-9 (MMP9) was increased, whereas the expression of epithelial marker E-cadherin was found to be decreased. In addition, expression of receptor activator of nuclear factor kappa-B ligand (RANKL), which is known to regulate MMP9 expression via Src activation, was also significantly increased after CXCL13 stimulation. Using specific protein kinase inhibitors, we confirmed that CXCL13 stimulated EMT and MMP9 expression via RANKL-Src axis in BC cell lines. To further validate this observation, we examined gene expression patterns in primary breast tumors and detected significantly higher expression of various mesenchymal markers and regulators in CXCL13-CXCR5 co-expressing patients</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24337540</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CYC1</Data></Cell>
    <Cell><Data ss:Type="String">CYC1 Silencing Sensitizes Osteosarcoma Cells to TRAIL-Induced Apoptosis</Data></Cell>
    <Cell><Data ss:Type="String">CYC1 plays an important role in OS tumorigenesis, and modulation of CYC1 may be an effective strategy to potentiate OS to apoptotic induction by TRAIL</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25562155</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CYC1</Data></Cell>
    <Cell><Data ss:Type="String">CYC1 Predicts Poor Prognosis in Patients with Breast Cancer</Data></Cell>
    <Cell><Data ss:Type="String">CYC1 plays crucial roles in breast cancer progression and might be a predictive factor assisting future patient diagnosis</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27239088</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CYC1</Data></Cell>
    <Cell><Data ss:Type="String">Genomic alterations underlie a pan-cancer metabolic shift associated with tumour hypoxia</Data></Cell>
    <Cell><Data ss:Type="String">These subtype-specific breast cancer metabolism signatures contained a common set of five genes (SQLE, PYCRL, TSTA3, CYC1 and SLC39A4) which were co-amplified with?MYC?on chromosome 8q24 and showed a positive correlation with hypoxia</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27358048</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CYC1</Data></Cell>
    <Cell><Data ss:Type="String">Cytochrome c1 in ductal carcinoma in situ of breast associated with proliferation and comedo necrosis</Data></Cell>
    <Cell><Data ss:Type="String">CYC1 plays important roles in cell proliferation and comedo necrosis through the elevated oxidative phosphorylation activity in human DCIS</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28394473</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CYP11A1</Data></Cell>
    <Cell><Data ss:Type="String">Population-based case-control study of CYP11A gene polymorphism and breast cancer risk</Data></Cell>
    <Cell><Data ss:Type="String">The TAAAA repeat polymorphism near the promoter region of the CYP11A gene may be an important susceptibility factor for breast cancer risk.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">15159300</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CYP11A1</Data></Cell>
    <Cell><Data ss:Type="String">Polymorphisms in steroid hormone biosynthesis genes and risk of breast cancer and fibrocystic breast conditions in Chinese women</Data></Cell>
    <Cell><Data ss:Type="String">Our findings support the possibility that common allelic variation at the CYP11A1 D15S520 locus alters breast cancer risk in Chinese women.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">18483327</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CYP11A1</Data></Cell>
    <Cell><Data ss:Type="String">Risk-Association of CYP11A1 Polymorphisms and Breast Cancer Among Han Chinese Women in Southern China</Data></Cell>
    <Cell><Data ss:Type="String">Polymorphisms of CYP11A1 are related to breast cancer susceptibility in Han Chinese women of South China.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22606018</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CYP19A1</Data></Cell>
    <Cell><Data ss:Type="String">Positive Association of Polymorphisms in Estrogen Biosynthesis Gene, CYP19A1, and Metabolism, GST, in Breast Cancer Susceptibility</Data></Cell>
    <Cell><Data ss:Type="String">The effect of CYP19A1 T/C polymorphism in susceptibility to breast cancer development can be modulated by the presence of GSTM1 and GSTT1, but not GSTP1</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22300440</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CYP19A1</Data></Cell>
    <Cell><Data ss:Type="String">SIRT1 positively regulates breast cancer associated human aromatase (CYP19A1) expression</Data></Cell>
    <Cell><Data ss:Type="String">SIRT1 occupies the promoter regions PI.3/PII and PI.4, and its inhibition leads to increased acetylation of estrogen-related receptor伪, a transcription factor that positively regulates CYP19A1 transcription in epithelial cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23340254</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CYP19A1</Data></Cell>
    <Cell><Data ss:Type="String">Influence of CYP19A1 polymorphisms on the treatment of breast cancer with aromatase inhibitors: a systematic review and meta-analysis</Data></Cell>
    <Cell><Data ss:Type="String">The effects of CYP19A1 polymorphisms on clinical outcomes were most often detected in individual studies, suggesting that longer-term studies will better clarify these associations</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26067721</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CYP19A1</Data></Cell>
    <Cell><Data ss:Type="String">The rs4646 and rs12592697 Polymorphisms in CYP19A1?Are Associated with Disease Progression among Patients with Breast Cancer from Different Racial/Ethnic Backgrounds</Data></Cell>
    <Cell><Data ss:Type="String">The rs4646 and the rs12592697 SNPs in CYP19A1 are associated with differences in disease progression in postmenopausal women. However, treatment appears to mitigate the differences in genetic risk.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27994616</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">CYP19A1</Data></Cell>
    <Cell><Data ss:Type="String">Acquired CYP19A1 amplification is an early specific mechanism of aromatase inhibitor resistance in ERα metastatic breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">AI treatment itself selects for acquired CYP19A1amp and promotes local autocrine estrogen signaling in AI-resistant metastatic patients</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28112739</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DCT</Data></Cell>
    <Cell><Data ss:Type="String">The Role of DCT/TYRP2 in Resistance of Melanoma Cells to Drugs and Radiation</Data></Cell>
    <Cell><Data ss:Type="String">Melanoma cells expressing very low levels of DCT are highly susceptible to either type of treatment. Overexpression of DCT in melanoma cells by transfection could confer both radioresistance and chemoresistance</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">Del-1</Data></Cell>
    <Cell><Data ss:Type="String">Exosomal Del-1 as a potent diagnostic marker for breast cancer: A prospective cohort study</Data></Cell>
    <Cell><Data ss:Type="String">As the current prospective cohort study demonstrated a normalization of exosomal Del-1 after curative surgery, exosomal Del-1 can be confirmed as a potent diagnostic biomarker for breast cancer. Plus, a high Del-1 level after surgery seems related with early relapse suggesting a potential prognostic marker by identifying the existence of residual tumor</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">Del-1</Data></Cell>
    <Cell><Data ss:Type="String">Identification of Developmental Endothelial Locus-1 on Circulating Extracellular Vesicles as a Novel Biomarker for Early Breast Cancer Detection.</Data></Cell>
    <Cell><Data ss:Type="String">Del-1 on circulating EVs is a promising marker to improve identification of patients with early-stage breast cancer and distinguish breast cancer from benign breast tumors and noncancerous diseases.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26603257</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">Del-1</Data></Cell>
    <Cell><Data ss:Type="String">Del-1 Expression as a Potential Biomarker in Triple-Negative Early Breast Cancer.</Data></Cell>
    <Cell><Data ss:Type="String">Based on its relationship to an unfavorable histology and worse survival trend, Del-1 could act as a molecular target in TNBC patients.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29393238</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">Del-1</Data></Cell>
    <Cell><Data ss:Type="String">Del-1 Expression as a Potential Biomarker in Triple-Negative Early Breast Cancer.</Data></Cell>
    <Cell><Data ss:Type="String">A correlation was found between Del-1 expression and an aggressive histological grade, nuclear mitosis, and polymorphism, suggesting a possible role in tumor progression.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29393238</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">Del-1</Data></Cell>
    <Cell><Data ss:Type="String">Exosomal Del-1 as a potent diagnostic marker for breast cancer: A prospective cohort study.</Data></Cell>
    <Cell><Data ss:Type="String">Exosomal Del-1 can be confirmed as a potent diagnostic biomarker for breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">Del-1</Data></Cell>
    <Cell><Data ss:Type="String">Del-1 promotes the proliferation and migration of tamoxifen-resistant MCF7 breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">The expression of Del-1 promote tamoxifen resistance in breast cancer celils and coud be a novel targed for anti-breast cancer treatment</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">Del-1</Data></Cell>
    <Cell><Data ss:Type="String">Del-1 promotes the proliferation and migration of tamoxifen-resistant MCF7 breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">Down-regulation of Del-1 inhibited the proliferation and migration of TAM MCF 7 cells. </Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">Dicer</Data></Cell>
    <Cell><Data ss:Type="String">Cancer Exosomes Perform Cell-Independent MicroRNA Biogenesis and Promote Tumorigenesis</Data></Cell>
    <Cell><Data ss:Type="String">Cancer exosomes induce tumor formation in a Dicer-dependent manner</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">25446899</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">Dicer</Data></Cell>
    <Cell><Data ss:Type="String">Prognostic value of Dicer expression in human breast cancers and association with the mesenchymal phenotype.</Data></Cell>
    <Cell><Data ss:Type="String">Assessment of Dicer expression may facilitate prediction of distant metastases for patients suffering from breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19672267</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">Dicer</Data></Cell>
    <Cell><Data ss:Type="String">Dysregulated expression of dicer and drosha in breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">The decreased expression of Dicer and Drosha may play a role in down-regulation of miRNAs in breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21898071</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">Dicer</Data></Cell>
    <Cell><Data ss:Type="String">Loss of Dicer expression is associated with breast cancer progression and recurrence.</Data></Cell>
    <Cell><Data ss:Type="String">Dicer protein plays a role in human BC progression and behaviour, and assessment of its expression could provide prognostic information in BC including the HER2-positive class.In invasive BC, loss of Dicer expression was associated with features of aggressive behaviour including higher histological grade, loss of hormone receptor and BRCA1 protein expression and with shorter disease-free survival (DFS). Moreover, loss of Dicer was predictive of better response to chemotherapy and to endocrine therapy.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22821364</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">Dicer</Data></Cell>
    <Cell><Data ss:Type="String">Prognostic Significance of Deregulated Dicer Expression in Breast Cancer</Data></Cell>
    <Cell><Data ss:Type="String">Dicer is an important prognostic marker in breast cancer and that its prognostic role may be subtype specific.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24386264</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DMRT1</Data></Cell>
    <Cell><Data ss:Type="String">Genomic and Expression Profiling of Human Spermatocytic Seminomas: Primary Spermatocyte as Tumorigenic Precursor and DMRT1 as Candidate Chromosome 9 Gene</Data></Cell>
    <Cell><Data ss:Type="String">Based on the region of amplification defined on 9p and the associated expression plus confirmatory immunohistochemistry, DMRT1 (a male-specific transcriptional regulator) was identified as a likely candidate gene for involvement in the development of spermatocytic seminomas</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">16397242</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DMRT1</Data></Cell>
    <Cell><Data ss:Type="String">Variants near DMRT1, TERT and ATF7IP are associated with testicular germ cell cancer</Data></Cell>
    <Cell><Data ss:Type="String">A locus on chromosome 9 (rs755383, OR=1.37, P=1.12x10(-23)), containing the sex determination gene DMRT1, which has been linked to teratoma susceptibility in mice</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">20543847</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DMRT1</Data></Cell>
    <Cell><Data ss:Type="String">A second independent locus within DMRT1 is associated with testicular germ cell tumor susceptibility</Data></Cell>
    <Cell><Data ss:Type="String">In combined analysis that mutually conditions on both DMRT1 single nucleotide polymorphism markers, TGCT cases had elevated odds of carriage of the rs7040024 major A allele [per-allele odds ratio (OR) = 1.48, 95% confidence interval (CI) 1.23, 1.78; P = 2.52 脳 10(-5)] compared with controls, while the association with rs755383 persisted (per allele OR = 1.26, 95% CI 1.08, 1.47, P = 0.0036)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21551455</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DMRT1</Data></Cell>
    <Cell><Data ss:Type="String">Associations between variants in?KITLG,?SPRY4,?BAK1, and?DMRT1?and pediatric germ cell tumors</Data></Cell>
    <Cell><Data ss:Type="String">Recent genome wide association studies have identified susceptibility loci for adult testicular germ cell tumors (GCT) near KITLG, SPRY4, BAK1, and DMRT1</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22072546</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DMRT1</Data></Cell>
    <Cell><Data ss:Type="String">Interaction between DMRT1 function and genetic background modulates signaling and pluripotency to control tumor susceptibility in the fetal germ line</Data></Cell>
    <Cell><Data ss:Type="String">Involvement of DMRT1 in human TGCT, the downstream genes and pathways identified in this study provide potentially useful candidates for roles in the human disease</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23473982</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DOK1</Data></Cell>
    <Cell><Data ss:Type="String">Characterization of DOK1, a candidate tumor suppressor gene, in epithelial ovarian cancer</Data></Cell>
    <Cell><Data ss:Type="String">These analyses were also indicative for DOK1 protective role in EOC tumorigenesis, linked to DOK1-mediated induction of some tumor suppressor factors and its suppression of pro-metastasis genes</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21856257</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DOK1</Data></Cell>
    <Cell><Data ss:Type="String">Transcriptional regulation of the human tumor suppressor DOK1 by E2F1</Data></Cell>
    <Cell><Data ss:Type="String">E2F1 is a key factor in DOK1 expression and provide novel insights into the regulation of these events in cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23028047</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DOK1</Data></Cell>
    <Cell><Data ss:Type="String">BRK Targets Dok1 for Ubiquitin-Mediated Proteasomal Degradation to Promote Cell Proliferation and Migration</Data></Cell>
    <Cell><Data ss:Type="String">A novel mechanism of action of BRK in the promotion of tumor formation, which involves the targeting of tumor suppressor Dok1 for degradation through the ubiquitin proteasomal pathway</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24523872</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DOK1</Data></Cell>
    <Cell><Data ss:Type="String">A crucial role for DOK1 in PDGF-BB-stimulated glioma cell invasion through p130Cas and Rap1 signalling</Data></Cell>
    <Cell><Data ss:Type="String">Knockdown of DOK1 and Rap1 inhibited PDGF-BB-induced chemotactic cell migration, and knockdown of DOK1 and Rap1 and expression of DOK1FF inhibited PDGF-mediated three-dimensional (3D) spheroid invasion</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24762811</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DOK1</Data></Cell>
    <Cell><Data ss:Type="String">Dok1 and Dok2 Proteins Regulate Cell Cycle in Hematopoietic Stem and Progenitor Cells</Data></Cell>
    <Cell><Data ss:Type="String">Dok1 and Dok2 proteins are involved in the control of hematopoietic stem cell cycle regulation</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27183638</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DOK1</Data></Cell>
    <Cell><Data ss:Type="String">Subcellular compartmentalization of docking protein-1 contributes to progression in colorectal cancer</Data></Cell>
    <Cell><Data ss:Type="String">DOK1 was identified as a prognostic factor for non-metastatic CRC, and, via its drugability by PPARγ-agonist, may constitute a potential target for future cancer treatments</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27428427</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DOK7</Data></Cell>
    <Cell><Data ss:Type="String">DNA methylation profiling in breast cancer discordant identical twins identifies DOK7 as novel epigenetic biomarker</Data></Cell>
    <Cell><Data ss:Type="String">Hypermethylation of DOK7 occurs years before tumor diagnosis, suggesting a role as a powerful epigenetic blood-based biomarker as well as providing insights into breast cancer pathogenesis.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23054610</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DOK7</Data></Cell>
    <Cell><Data ss:Type="String">The downstream of tyrosine kinase 7 is reduced in lung cancer and is associated with poor survival of patients with lung cancer.</Data></Cell>
    <Cell><Data ss:Type="String">DOK7 was reduced in lung cancer and reduced DOK7 expression was associated with poorer survival. </Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28393246</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DOK7</Data></Cell>
    <Cell><Data ss:Type="String">The downstream of tyrosine kinase 7 is reduced in lung cancer and is associated with poor survival of patients with lung cancer.</Data></Cell>
    <Cell><Data ss:Type="String">DOK7 isoform 1 plays an inhibitory role on the proliferation and migration of lung cancer cells in which Akt pathway may be involved.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28393246</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DOK7</Data></Cell>
    <Cell><Data ss:Type="String">Evidence for Tumour Suppressor Function of DOK7 in Human Breast Cancer</Data></Cell>
    <Cell><Data ss:Type="String">Higher DOK-7 expression was correlated with longer disease free and overall survival times.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DTX3L</Data></Cell>
    <Cell><Data ss:Type="String">DTX3L and ARTD9 inhibit IRF1 expression and mediate in cooperation with ARTD8 survival and proliferation of metastatic prostate cancer cells.</Data></Cell>
    <Cell><Data ss:Type="String">Our data strongly indicate that a crosstalk between STAT1, DTX3L and ARTD-like mono-ADP-ribosyltransferases mediates proliferation and survival of  metastatic Pca(mPCa) cells.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24886089</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DTX3L</Data></Cell>
    <Cell><Data ss:Type="String">DTX3L and ARTD9 inhibit IRF1 expression and mediate in cooperation with ARTD8 survival and proliferation of metastatic prostate cancer cells.</Data></Cell>
    <Cell><Data ss:Type="String">DTX3L and ARTD9 act together as repressors of the tumor suppressor IRF1 in mPCa cells. Furthermore, the present study shows that DTX3L together with STAT1 and STAT3 is implicated in cell migration of mPCa cells.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24886089</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DTX3L</Data></Cell>
    <Cell><Data ss:Type="String">DTX3L is upregulated in glioma and is associated with glioma progression.</Data></Cell>
    <Cell><Data ss:Type="String">DTX3L could be a potential prognostic biomarker for glioma.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28627634</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DTX3L</Data></Cell>
    <Cell><Data ss:Type="String">DTX3L is upregulated in glioma and is associated with glioma progression.</Data></Cell>
    <Cell><Data ss:Type="String">Knockdown of DTX3L by siRNA transfection increased glioma cell apoptosis. Moreover, suppression of DTX3L expression was shown to significantly inhibit the migration and invasion of glioma cells. </Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28627634</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DUSP1</Data></Cell>
    <Cell><Data ss:Type="String">DUSP1 is a novel target for enhancing pancreatic cancer cell sensitivity to gemcitabine</Data></Cell>
    <Cell><Data ss:Type="String">Gemcitabine-mediated upregulation of DUSP1 contributes to a negative feedback loop that attenuates its beneficial actions on stress pathways and apoptosis, raising the possibility that targeting DUSP1 in PDAC may have the advantage of enhancing gemcitabine chemosensitivity while suppressing angiogenesis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24409315</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DUSP1</Data></Cell>
    <Cell><Data ss:Type="String">Role of DUSP1/MKP1 in tumorigenesis, tumor progression and therapy</Data></Cell>
    <Cell><Data ss:Type="String">As a protein phosphatase, DUSP1 also downregulates p38?MAPKs and?JNKs signaling through directly dephosphorylating threonine and tyrosine. It has been detected that?DUSP1 is involved in various functions, including proliferation, differentiation, and apoptosis in normal cells. In various human cancers, abnormal expression of?DUSP1 was observed which was associated with prognosis of tumor patients</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27227569</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DUSP1</Data></Cell>
    <Cell><Data ss:Type="String">DUSP1 inhibits cell proliferation, metastasis and invasion and angiogenesis in gallbladder cancer</Data></Cell>
    <Cell><Data ss:Type="String">The DUSP1-pERK-MMP2/VEGF signals may provide new biomarkers and/or therapeutic targets to better suppress GBC metastasis in the future</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28129656</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DUSP1</Data></Cell>
    <Cell><Data ss:Type="String">DUSP1 enhances the chemoresistance of gallbladder cancer via the modulation of the p38 pathway and DNA damage/repair system</Data></Cell>
    <Cell><Data ss:Type="String">DUSP1 may be a promising target to overcome chemoresistance in GBC therapy</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30008878</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">DUSP1</Data></Cell>
    <Cell><Data ss:Type="String">DUSP1 is involved in the progression of small cell carcinoma of the prostate</Data></Cell>
    <Cell><Data ss:Type="String">DUSP1 is involved in the progression of SCCP and may provide a new therapeutic target for SCCP treatment</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30108432</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">EEF1A1</Data></Cell>
    <Cell><Data ss:Type="String">Characterization of RNA in exosomes secreted by human breast cancer cell lines using next-generation sequencing</Data></Cell>
    <Cell><Data ss:Type="String">EEF1A1 distinguish exosomes produced by low metastatic breast cancer cell line (MDA-MB-436) from that produced by highly metastatic breast cancer cell line (MDA-MB-231)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">24255815</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">EEF1A1</Data></Cell>
    <Cell><Data ss:Type="String">Dissecting the expression of EEF1A1/2 genes in human prostate cancer cells: the potential of EEF1A2 as a hallmark for prostate transformation and progression</Data></Cell>
    <Cell><Data ss:Type="String">Eukaryotic elongation factor 1A2 switch-on, observed in cultured tumour prostate cells and in human prostate tumour samples, may represent a feature of prostate cancer; in contrast, a minor involvement is assigned to EEF1A1</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22095224</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">EEF1A1</Data></Cell>
    <Cell><Data ss:Type="String">P21 activated kinase 4 binds translation elongation factor eEF1A1 to promote gastric cancer cell migration and invasion</Data></Cell>
    <Cell><Data ss:Type="String">PAK4 interacted with eEF1A1 to promote migration and invasion of gastric cancer cells, thereby providing new insights into the function of PAK4 and eEF1A1 in the progression of gastric cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28393218</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">EEF1A1</Data></Cell>
    <Cell><Data ss:Type="String">Contradictory mRNA and protein misexpression of EEF1A1 in ductal breast carcinoma due to cell cycle regulation and cellular stress</Data></Cell>
    <Cell><Data ss:Type="String">EEF1A1 mRNA levels in breast carcinomas are low due to EEF1A1 allelic copy number loss, found in 27% of tumors, and cell cycle-specific expression, because mRNA levels are high in G1 and low in proliferating cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30224719</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">EEF1A1</Data></Cell>
    <Cell><Data ss:Type="String">Genome-wide target interactome profiling reveals a novel EEF1A1 epigenetic pathway for oncogenic lncRNA MALAT1 in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Knockdown of MALAT1 reduced cell proliferation and invasion by arresting cells at the G0/G1 phase. Ectopic overexpression of EEF1A1 reversed the altered tumor phenotypes induced by MALAT1 shRNA treatment</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31105998</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">EEF1A1</Data></Cell>
    <Cell><Data ss:Type="String">Isoforms of elongation factor eEF1A may be differently regulated at post-transcriptional level in breast cancer progression</Data></Cell>
    <Cell><Data ss:Type="String">EEF1A1 and EEF1A2 mRNAs contain distinct motifs in the UTRs and are differently regulated in cancer suggesting the possibility of their control by different cellular signals</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ELK1</Data></Cell>
    <Cell><Data ss:Type="String">Estrogen Receptor-mediated Activation of the Serum Response Element in MCF-7 Cells through MAPK-dependent Phosphorylation of Elk-1</Data></Cell>
    <Cell><Data ss:Type="String">Transcriptional activation of the SRE by E2 was due to ERα activation of the MAPK pathway and increased binding of the serum response factor and Elk-1 to the SRE.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">11145955</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ELK1</Data></Cell>
    <Cell><Data ss:Type="String">c-Fos oncogene regulator Elk-1 interacts with BRCA1 splice variants BRCA1a/1b and enhances BRCA1a/1b-mediated growth suppression in breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">BRCA1a/1b proteins function as growth/tumor suppressors is through inhibition of the expression of Elk-1 target genes like c-Fos</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">11313879</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ELK1</Data></Cell>
    <Cell><Data ss:Type="String">Genome-Wide Analysis Reveals PADI4 Cooperates with Elk-1 to Activate?c-Fos?Expression in Breast Cancer Cells</Data></Cell>
    <Cell><Data ss:Type="String">PADI4 interacts with Elk-1 at the c-Fos promoter and that, following Epidermal Growth Factor (EGF) stimulation, PADI4 catalytic activity facilitates Elk-1 phosphorylation, histone H4 acetylation, and c-Fos transcriptional activation.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21655091</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ELK1</Data></Cell>
    <Cell><Data ss:Type="String">Tumor-suppressive miRNA-135a inhibits breast cancer cell proliferation by targeting ELK1 and ELK3 oncogenes</Data></Cell>
    <Cell><Data ss:Type="String">MiR-135a regulates cell proliferation in breast cancer by targeting ELK1 and ELK3 oncogenes, and suggests that miR-135a potentially can act as a tumor suppressor</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29892795</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ELK1</Data></Cell>
    <Cell><Data ss:Type="String">Suppression of Elk1 inhibits thyroid cancer progression by mediating PTEN expression</Data></Cell>
    <Cell><Data ss:Type="String">Elk1 inhibition induced thyroid cancer cell apoptosis and restrained their proliferation by regulating Egr-1/PTEN, indicating a potential role for Elk1 in thyroid cancer treatment</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30015900</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ENPP1</Data></Cell>
    <Cell><Data ss:Type="String">Enpp1: A Potential Facilitator of Breast Cancer Bone Metastasis</Data></Cell>
    <Cell><Data ss:Type="String">By both routes of administration, increased expression of Enpp1 enhanced the ability of MDA-MB-231 cells to form tumors in the bone relative to cells expressing vector alone, as determined by digital radiography and histological analysis锛泃hese data suggest a potential role for Enpp1 in the development of breast cancer bone metastasis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23861746</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ENPP1</Data></Cell>
    <Cell><Data ss:Type="String">Identification of Gene Expression Signature in Estrogen Receptor Positive Breast Carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">Significant over-expression of all the six genes in ERα (+) breast tumors as compared to ERα (-) breast tumors. In vitro studies using T-47D breast cancer cell line confirmed the estrogen dependant expression of four of the above six genes (SLC7A8, ENPP1, LAMB2, and PLAT)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24179381</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ENPP1</Data></Cell>
    <Cell><Data ss:Type="String">Functional characterization of ENPP1 reveals a link between cell cycle progression and stem-like phenotype in glioblastoma</Data></Cell>
    <Cell><Data ss:Type="String">A high-throughput phenotypic screen in glioblastoma stem-like cells (GSCs) identified a novel molecular mechanism in which ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1) plays an important role in balancing the pool of nucleotides, thus maintaining GSCs in an undifferentiated proliferative state</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27308351</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ENPP1</Data></Cell>
    <Cell><Data ss:Type="String">Functional characterization of ENPP1 reveals a link between cell cycle progression and stem-like phenotype in glioblastoma</Data></Cell>
    <Cell><Data ss:Type="String">A novel molecular mechanism in which ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1) plays an important role in balancing the pool of nucleotides, thus maintaining GSCs in an undifferentiated proliferative state</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27308351</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ENPP1</Data></Cell>
    <Cell><Data ss:Type="String">Development of an ENPP1 Fluorescence Probe for Inhibitor Screening, Cellular Imaging, and Prognostic Assessment of Malignant Breast Cancer</Data></Cell>
    <Cell><Data ss:Type="String">ENPP1 mRNA expression in tissue samples from patients with triple-negative breast cancer was significantly inversely related to recurrence-free survival (RFS) and overall survival (OS)</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31536342</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">EPCAM</Data></Cell>
    <Cell><Data ss:Type="String">Tumour exosomes inhibit binding of tumour-reactive antibodies to tumour cells and reduce ADCC</Data></Cell>
    <Cell><Data ss:Type="String">Tumour-derived exosomes interfere with the tumour-specific function of immune cells and constitute an additional mechanism how tumours escape from immune surveillance</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">21293856</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">EPCAM</Data></Cell>
    <Cell><Data ss:Type="String">Epithelial-to-mesenchymal transition induced by TGF-β1 is mediated by AP1-dependent EpCAM expression in MCF-7 cells</Data></Cell>
    <Cell><Data ss:Type="String">EpCAM may be an attractive strategy to treat breast cancer.This study implicates the potential value of EpCAM as a molecular marker for breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25205054</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">EPCAM</Data></Cell>
    <Cell><Data ss:Type="String">Epithelial-to-mesenchymal transition induced by TGF-β1 is mediated by AP1-dependent EpCAM expression in MCF-7 cells</Data></Cell>
    <Cell><Data ss:Type="String">EpCAM participated in TGF-β1-induced EMT. TGF-β1 treatment of MCF-7 breast cancer cells was shown to induce EpCAM expression, which promoted the EMT and cell migration. EpCAM overexpression further enhanced TGF-β1-induced EMT and EpCAM knockdown inhibited TGF-β1-induced EMT. We further demonstrated that TGF-β1 treatment induced the phosphorylation of JNK that was in turn responsible for the increased expression of Jun and Fos. This result suggests an important role of the JNK to AP-1 signaling to EpCAM downstream of TGF-β1 for the induction of EMT in the breast cancer cells.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25205054</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">EPCAM</Data></Cell>
    <Cell><Data ss:Type="String">By inhibiting Ras/Raf/ERK and MMP-9, knockdown of EpCAM inhibits breast cancer cell growth and metastasis</Data></Cell>
    <Cell><Data ss:Type="String">Overexpression of EpCAM in breast cancer cells enhanced tumor cell growth in vitro and increased invasiveness, whereas small interfering RNA-mediated silencing of EpCAM (si-EpCAM) had the opposite effect. EpCAM knockdown led to decreased phosphorylation of Raf and ERK, suppression of malignant behavior of breast cancer cells, and inhibition of the Ras/Raf/ERK signaling pathway.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26356670</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">EPCAM</Data></Cell>
    <Cell><Data ss:Type="String">EpCAM and COX?2 expression are positively correlated in human breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">EpCAM may serve a role in the regulation of cancer cell growth and may hold potential as a prognostic marker in breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28393249</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ERBB2</Data></Cell>
    <Cell><Data ss:Type="String">Tumour exosomes inhibit binding of tumour-reactive antibodies to tumour cells and reduce ADCC</Data></Cell>
    <Cell><Data ss:Type="String">Tumour-derived exosomes interfere with the tumour-specific function of immune cells and constitute an additional mechanism how tumours escape from immune surveillance</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">21293856</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ERBB2</Data></Cell>
    <Cell><Data ss:Type="String">Genetic alterations in ERBB2-amplified breast carcinomas</Data></Cell>
    <Cell><Data ss:Type="String">Breast tumors showing erbB2 overexpression or gene amplification are genetically distinct from erbB2-negative tumors</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">10632352</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ERBB2</Data></Cell>
    <Cell><Data ss:Type="String">ERBB2 and TOP2A in Breast Cancer: A Comprehensive Analysis of Gene Amplification, RNA Levels, and Protein Expression and Their Influence on Prognosis and Prediction</Data></Cell>
    <Cell><Data ss:Type="String">ERBB2 gene expression was associated with the MFI only in estrogen receptor-positive carcinomas, whereas ERBB2 protein expression (P = 0.032) was associated with MFI in the entire cohort</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">20371687</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ERBB2</Data></Cell>
    <Cell><Data ss:Type="String">The extracellular domain of Her2 in serum as a biomarker of breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">SHER2 ECD should be considered as a promising biomarker to detect cancer recurrence and metastasis</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29491426</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ERBB2</Data></Cell>
    <Cell><Data ss:Type="String">Targeting promiscuous heterodimerization overcomes innate resistance to ERBB2 dimerization inhibitors in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">The interaction of ERBB2 with a number of non-canonical RTKs activates a compensatory signalling response following treatment with pertuzumab, although a counter-intuitive combination of ERBB2 antibody therapy and a kinase inhibitor can overcome this innate therapeutic resistance</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30898150</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FAM162A</Data></Cell>
    <Cell><Data ss:Type="String">The usability of a 15-gene hypoxia classifier as a universal hypoxia profile in various cancer cell types</Data></Cell>
    <Cell><Data ss:Type="String">The gene expression analysis demonstrated cell line specific differences in the hypoxia response of the 15 genes, with BNIP3 not being upregulated at hypoxic conditions in 3 out of 6 colon cancer cell lines, and ALDOA in OE21 and FAM162A and SLC2A1 in SW116 only showing limited hypoxia induction</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26169282</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FAM87A</Data></Cell>
    <Cell><Data ss:Type="String">Comprehensive analysis of lncRNA-associated competing endogenous RNA network in tongue squamous cell carcinoma</Data></Cell>
    <Cell><Data ss:Type="String"> FAM87A was identified as novel, potential prognostic biomarkers and therapeutic targets for  tongue squamous cell carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30755833</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FAM87A</Data></Cell>
    <Cell><Data ss:Type="String">CNV Primed lncRNAs Deregulation Contributes to Poor Prognosis in Colorectal Cancer</Data></Cell>
    <Cell><Data ss:Type="String">Comparing lncRNAs expression patterns between copy-deleted or copy-amplified and the normal samples, we identify 9 lncRNAs(FAM87A, LOC101927752, KBTBD11-OT1, LOC100287015, LOC101929066, CASC11, HM13-AS1, ABALON, NKILA),?</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FGF9</Data></Cell>
    <Cell><Data ss:Type="String">Estrogen expands breast cancer stem-like cells through paracrine FGF/Tbx3 signaling</Data></Cell>
    <Cell><Data ss:Type="String">Estrogen or FGF9 pretreatment induced CSC properties of breast cancer cell lines and freshly isolated breast cancer cells, whereas cotreatment of cells with tamoxifen or a small molecule inhibitor of FGFR signaling was sufficient to prevent the estrogen-induced expansion of CSCs</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21098263</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FGF9</Data></Cell>
    <Cell><Data ss:Type="String">Expression of fibroblast growth factor 9 is associated with poor prognosis in patients with resected non-small cell lung cancer</Data></Cell>
    <Cell><Data ss:Type="String">FGF9 may be a novel unfavorable prognostic indicator and a candidate therapeutic target of NSCLC</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24239165</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FGF9</Data></Cell>
    <Cell><Data ss:Type="String">FGF9 from cancer-associated fibroblasts is a possible mediator of invasion and anti-apoptosis of gastric cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">FGF9 is a possible mediator secreted by CAFs that promotes the anti-apoptosis and invasive capability of gastric cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25925261</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FGF9</Data></Cell>
    <Cell><Data ss:Type="String">The anti-apoptotic and prognostic value of fibroblast growth factor 9 in gastric cancer</Data></Cell>
    <Cell><Data ss:Type="String">FGF9 may provide the anti-apoptotic function and be useful as a novel independent marker for evaluating GC prognosis</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27166269</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FGF9</Data></Cell>
    <Cell><Data ss:Type="String">FGF9/FGFR2 increase cell proliferation by activating ERK1/2, Rb/E2F1, and cell cycle pathways in mouse Leydig tumor cells</Data></Cell>
    <Cell><Data ss:Type="String">FGF9 interacts with FGFR2 to activate ERK1/2, Rb/E2F1 and cell cycle pathways to induce MA-10 cell proliferation in?vitro and tumor growth in vivo</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30191630</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FGFR2</Data></Cell>
    <Cell><Data ss:Type="String">Proteomic Profiling of Exosomes Secreted by Breast Cancer Cells with Varying Metastatic Potential</Data></Cell>
    <Cell><Data ss:Type="String">Presumably aid in targeting the primary cancer cells to specific metastatic sites</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29115712</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FGFR2</Data></Cell>
    <Cell><Data ss:Type="String">The Breast Cancer Susceptibility Gene Product Fibroblast Growth Factor Receptor 2 Serves as a Scaffold for Regulation of NF-κB Signaling</Data></Cell>
    <Cell><Data ss:Type="String">FGFR2 serves as a scaffold for multiple components of the NF-κB signaling complex</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22988296</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FGFR2</Data></Cell>
    <Cell><Data ss:Type="String">Activating somatic FGFR2 mutations in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Somatic breast cancer mutations in FGFR2 providing evidence for the activating nature of FGFR2-mediated signalling in the pathogenesis of breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23527311</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FGFR2</Data></Cell>
    <Cell><Data ss:Type="String">Master regulators of FGFR2 signalling and breast cancer risk</Data></Cell>
    <Cell><Data ss:Type="String">Fibroblast growth factor receptor 2 signalling has an important role in mediating breast cancer risk</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24043118</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FGFR2</Data></Cell>
    <Cell><Data ss:Type="String">FGFR2 amplification in metastatic hormone-positive breast cancer and response to an mTOR inhibitor</Data></Cell>
    <Cell><Data ss:Type="String">GFR2 amplification to treatment with nab-paclitaxel and an mTOR inhibitor, whilst showing no significant benefit from endocrine therapy or treatment with a CDK4/6 inhibitor</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28430863</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FGFR2</Data></Cell>
    <Cell><Data ss:Type="String">FGFR2 risk SNPs confer breast cancer risk by augmenting oestrogen responsiveness</Data></Cell>
    <Cell><Data ss:Type="String">FGFR2 can confer increased breast cancer risk that is consistent with oestrogen exposure as a major driver of breast cancer risk</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27236187</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FGFR2</Data></Cell>
    <Cell><Data ss:Type="String">Association of FGFR2 and TOX3 Genetic Variants With the Risk of Breast Cancer in Iranian Women</Data></Cell>
    <Cell><Data ss:Type="String">Genetic variants of FGFR2 (rs1219648 AG) and TOX3 (rs8051542 TC) can be potential candidate biomarkers for breast cancer risk</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FGFR3</Data></Cell>
    <Cell><Data ss:Type="String">Proteomic Profiling of Exosomes Secreted by Breast Cancer Cells with Varying Metastatic Potential</Data></Cell>
    <Cell><Data ss:Type="String">Presumably aid in targeting the primary cancer cells to specific metastatic sites</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29115712</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FGFR3</Data></Cell>
    <Cell><Data ss:Type="String">Frequent activating mutations of FGFR3 in human bladder and cervix carcinomas</Data></Cell>
    <Cell><Data ss:Type="String">Genomic alterations of FGFR3 are among the best described oncogenic pathway in UC</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">10471491</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FGFR3</Data></Cell>
    <Cell><Data ss:Type="String">Immunohistochemical detection of fibroblast growth factor receptor 3 in human breast cancer: correlation with clinicopathological/molecular parameters and prognosis</Data></Cell>
    <Cell><Data ss:Type="String">FGFR3 expression in invasive breast cancer was not found to be significantly associated with specific clinicopathological/molecular parameters, but might be used as a candidate marker for a poor prognosis</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21116113</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FGFR3</Data></Cell>
    <Cell><Data ss:Type="String">Mechanisms of FGFR3 actions in endocrine resistant breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">FGFR3 activation in MCF7 cells stimulated activation of the mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K) signalling pathways, both of which have been implicated in tamoxifen resistance in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21792889</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FGFR3</Data></Cell>
    <Cell><Data ss:Type="String">FGF receptor genes and breast cancer susceptibility: results from the Breast Cancer Association Consortium</Data></Cell>
    <Cell><Data ss:Type="String">Some SNPs in FGFR3 gene were closely related to breast cancer risk</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24548884</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FIBP</Data></Cell>
    <Cell><Data ss:Type="String">Proteomic Profiling of Exosomes Secreted by Breast Cancer Cells with Varying Metastatic Potential</Data></Cell>
    <Cell><Data ss:Type="String">Presumably aid in targeting the primary cancer cells to specific metastatic sites</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29115712</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FIBP</Data></Cell>
    <Cell><Data ss:Type="String">Proteomic Analysis of the Human Cyclin-dependent Kinase Family Reveals a Novel CDK5 Complex Involved in Cell Growth and Migration</Data></Cell>
    <Cell><Data ss:Type="String">CDK5-, KIAA0528-, or FIBP-depleted breast cancer cells displayed impaired proliferation and decreased migration, suggesting that this complex is required for cell growth and migration in non-neural cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25096995</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FIBP</Data></Cell>
    <Cell><Data ss:Type="String">A recessive syndrome of intellectual disability, moderate overgrowth, and renal dysplasia predisposing to Wilms tumor is caused by a mutation in FIBP gene</Data></Cell>
    <Cell><Data ss:Type="String">These findings provide convincing evidence implicating FIBP aberrations in the newly recognized overgrowth syndrome and expand the associated phenotypes to include possible Wilms tumor predisposition</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27183861</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FIBP</Data></Cell>
    <Cell><Data ss:Type="String">FIBP knockdown attenuates growth and enhances chemotherapy in colorectal cancer via regulating GSK3β-related pathways</Data></Cell>
    <Cell><Data ss:Type="String">DNA methylation profiling suggested that FIBP regulated the stemness of CRC cells via methylation activity that was dependent on GSK3β but independent of β-catenin signaling</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30275459</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FRS2</Data></Cell>
    <Cell><Data ss:Type="String">Proteomic Profiling of Exosomes Secreted by Breast Cancer Cells with Varying Metastatic Potential</Data></Cell>
    <Cell><Data ss:Type="String">Presumably aid in targeting the primary cancer cells to specific metastatic sites</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29115712</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FRS2</Data></Cell>
    <Cell><Data ss:Type="String">MiR-4653-3p and its target gene FRS2 are prognostic biomarkers for hormone receptor positive breast cancer patients receiving tamoxifen as adjuvant endocrine therapy</Data></Cell>
    <Cell><Data ss:Type="String">MiR-4653-3p and its target gene FRS2 are prognostic biomarkers for hormone receptor-positive breast cancer patients receiving tamoxifen as an adjuvant endocrine therapy</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27533459</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FRS2</Data></Cell>
    <Cell><Data ss:Type="String">MiR-4653-3p and its target gene FRS2 are prognostic biomarkers for hormone receptor positive breast cancer patients receiving tamoxifen as adjuvant endocrine therapy</Data></Cell>
    <Cell><Data ss:Type="String">Fibroblast growth factor receptor substrate 2 (FRS2, also known as FRS2alpha) is a member of the adaptor/scaffold protein family. It was considered as an essential-conning center in FGFR signaling . FSR2 binds through its N-terminal phosphotyrosine-binding domain (PTB) to FGFR, resulting in phosphorylation of multiple tyrosine residues of FRS2 and subsequent activation of the downstream signaling (e.g., RAS/MAPK/ERK, PI3K/AKT/mTOR) and ubiquitination/degradation pathways . FRS2 acts as an oncogene in a variety of cancers, which regulates tumor cell differentiation, proliferation, and tumorigenesis . Inhibition of FRS2 could block the FGFR signaling and downstream biological functions</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27533459</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FRS2</Data></Cell>
    <Cell><Data ss:Type="String">Targeting FGFR pathway in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Activated FRS2 promotes downstream signaling through the RAS-mitogen-activated protein kinase (MAPK) or the phosphoinositide 3-kinase (PI3K)-AKT pathways that regulate cell proliferation, differentiation, and survival</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29156384</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FTH1</Data></Cell>
    <Cell><Data ss:Type="String">Characterization of RNA in exosomes secreted by human breast cancer cell lines using next-generation sequencing</Data></Cell>
    <Cell><Data ss:Type="String">FTH1 distinguish exosomes produced by low metastatic breast cancer cell line (MDA-MB-436) from that produced by highly metastatic breast cancer cell line (MDA-MB-231)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">24255815</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FTH1</Data></Cell>
    <Cell><Data ss:Type="String">Ferritin binds and activates p53 under oxidative stress</Data></Cell>
    <Cell><Data ss:Type="String">Our findings show that ferroxidase activity is not required for FTH1 to increase p53 transcriptional activity</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19716362</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FTH1</Data></Cell>
    <Cell><Data ss:Type="String">Ferritin heavy chain in triple negative breast cancer: a favorable prognostic marker that relates to a cluster of differentiation 8 positive (CD8+) effector T-cell response</Data></Cell>
    <Cell><Data ss:Type="String">Our data provide evidence toward new immune regulatory properties of FTH1 in TNBC, which may facilitate development of novel therapeutic targets</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24742827</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FTH1</Data></Cell>
    <Cell><Data ss:Type="String">Regulation of iron homeostasis by the p53-ISCU pathway</Data></Cell>
    <Cell><Data ss:Type="String">In response to DNA damage, p53 induced FTH1 and suppressed transferrin receptor, which regulates iron entry into cells. HCT116 p53+/+ cells were resistant to iron accumulation, but HCT116 p53 / cells accumulated intracellular iron after DNA damage</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26560363</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FTH1</Data></Cell>
    <Cell><Data ss:Type="String">Decreased Iron in Cancer Cells and Their Microenvironment Improves Cytolysis of Breast Cancer Cells by Natural Killer Cells</Data></Cell>
    <Cell><Data ss:Type="String">Real time quantitative polymerase chain reaction showed that iron up-regulated the expression of FTH1 and iron chelator DFOM reduced FTH1 expression of MCF-7 and MDA-MB-231 cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28476795</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FTH1</Data></Cell>
    <Cell><Data ss:Type="String">A FTH1 gene:pseudogene:microRNA network regulates tumorigenesis in prostate cancer</Data></Cell>
    <Cell><Data ss:Type="String">?In this study, we utilize an unbiased screen to identify the ferritin heavy chain 1 (FTH1) transcript and multiple FTH1 pseudogenes as targets of several oncogenic miRNAs in prostate cancer (PCa). We characterize the critical role of this FTH1 gene:pseudogene:miRNA network in regulating tumorigenesis in PCa, whereby oncogenic miRNAs downregulate the expression of FTH1 and its pseudogenes to drive oncogenesis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29240947</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FTL</Data></Cell>
    <Cell><Data ss:Type="String">Characterization of RNA in exosomes secreted by human breast cancer cell lines using next-generation sequencing</Data></Cell>
    <Cell><Data ss:Type="String">FTL distinguish exosomes produced by low metastatic breast cancer cell line (MDA-MB-436) from that produced by highly metastatic breast cancer cell line (MDA-MB-231)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">24255815</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FTL</Data></Cell>
    <Cell><Data ss:Type="String">Validation of tumor-associated macrophage ferritin light chain as a prognostic biomarker in node-negative breast cancer tumors: A multicentric 2004 national PHRC study</Data></Cell>
    <Cell><Data ss:Type="String">The validation of FTL as a breast tumor prognostic biomarker in node-negative patients, and second, the fact that FTL is stored in TAM</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21898387</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FTL</Data></Cell>
    <Cell><Data ss:Type="String">Iron metabolism disturbances in the MCF-7 human breast cancer cells with acquired resistance to doxorubicin and cisplatin</Data></Cell>
    <Cell><Data ss:Type="String">The increased levels of FTL in breast cancer indicate that FTL may be used as a diagnostic and prognostic marker for breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23969999</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FTL</Data></Cell>
    <Cell><Data ss:Type="String">Iron metabolism disturbances in the MCF-7 human breast cancer cells with acquired resistance to doxorubicin and cisplatin</Data></Cell>
    <Cell><Data ss:Type="String">Targeted downregulation of FTL protein by the microRNA miR-133a increases sensitivity of MCF-7/DOX and MCF-7/CDDP cells to doxorubicin and cisplatin</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23969999</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FTL</Data></Cell>
    <Cell><Data ss:Type="String">Ferritin Heavy Chain in Triple Negative Breast Cancer: A Favorable Prognostic Marker that Relates to a Cluster of Differentiation 8 Positive (CD8+) Effector T-cell Response</Data></Cell>
    <Cell><Data ss:Type="String">We observed that protein expression of FTH1 was significantly higher in good prognostic patients (n = 82) than those with poor prognosis (n = 44) (p = 0.001), whereas neither expression of FTL (p = 0.054) nor FTH1/FTL ratio (p = 0.566) showed significant difference between patients with different clinical outcome</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24742827</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FTL</Data></Cell>
    <Cell><Data ss:Type="String">Expression of Ferritin Light Chain (FTL) Is Elevated in Glioblastoma, and FTL Silencing Inhibits Glioblastoma Cell Proliferation via the GADD45/JNK Pathway</Data></Cell>
    <Cell><Data ss:Type="String">FTL regulates the growth of GBM cells via the GADD45/JNK pathway</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26871431</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FZD5</Data></Cell>
    <Cell><Data ss:Type="String">Expression and regulation of WNT5A and WNT5B in human cancer: Up-regulation of WNT5A by TNFα in MKN45 cells and up-regulation of WNT5B by β-estradiol in MCF-7 cells</Data></Cell>
    <Cell><Data ss:Type="String">Up-regulation of WNT5A and WNT5B in several types of human cancer expressing FZD5 might lead to more malignant phenotype through activation of the β-catenin - TCF pathway</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">12165812</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FZD5</Data></Cell>
    <Cell><Data ss:Type="String">Microrna-224 inhibits proliferation and migration of breast cancer cells by down-regulating fizzled 5 expression</Data></Cell>
    <Cell><Data ss:Type="String">MiR-224 inhibited cell proliferation and migration by targeting FZD5 and inhibiting WNT/β-catenin signaling in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27323393</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FZD5</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-671-3p inhibits the development of breast cancer: A study based on in vitro experiments, in-house quantitative polymerase chain reaction and bioinformatics analysis</Data></Cell>
    <Cell><Data ss:Type="String">WNT3A, CCND2, SFRP1, PRICKLE2, FZD5 and FZD4 were markedly downregulated in BC, suggesting that they may function as tumor suppressor genes in this tumor</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29620195</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">FZD5</Data></Cell>
    <Cell><Data ss:Type="String">Role of WNT5A receptors FZD5 and RYK in prostate cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">WNT5A/FZD5 and WNT5A/RYK signaling are both involved in mediating the pro-apoptotic and anti-proliferative effects of WNT5A in prostate cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29930766</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GATA4</Data></Cell>
    <Cell><Data ss:Type="String">A Negative Feedback Regulatory Loop Associates the Tyrosine Kinase Receptor ERBB2 and the Transcription Factor GATA4 in Breast Cancer Cells</Data></Cell>
    <Cell><Data ss:Type="String">In agreement with a repressor role of GATA4 on ERBB2 gene expression balanced by ERBB2 activation of the GATA4 gene, a negative correlation between the relative levels of ERBB2 and GATA4 mRNA was observed in breast cancer cell lines and breast tumor samples</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19276186</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GATA4</Data></Cell>
    <Cell><Data ss:Type="String">GATA4 promotes hepatoblastoma cell proliferation by altering expression of miR125b and DKK3</Data></Cell>
    <Cell><Data ss:Type="String">GATA4 is therefore a potential therapeutic target or biomarker for progression in HB patients</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27788486</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GATA4</Data></Cell>
    <Cell><Data ss:Type="String">GATA4 promotes hepatoblastoma cell proliferation by altering expression of miR125b and DKK3</Data></Cell>
    <Cell><Data ss:Type="String">GATA4/miR125b/DKK3 axis may be a major regulator of growth, migration, invasion, and survival in hepatoma cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27788486</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GATA4</Data></Cell>
    <Cell><Data ss:Type="String">GATA4 loss of function in liver cancer impedes precursor to hepatocyte transition</Data></Cell>
    <Cell><Data ss:Type="String">Thus, disruption of GATA4-mediated transactivation in HCC suppresses hepatocyte epithelial differentiation to sustain replicative precursor phenotype</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28758902</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GATA4</Data></Cell>
    <Cell><Data ss:Type="String">GATA4 inhibits cell differentiation and proliferation in pancreatic cancer</Data></Cell>
    <Cell><Data ss:Type="String">GATA4 gene might play a role in cell proliferation and differentiation during the progression of pancreatic cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30142155</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GATA4</Data></Cell>
    <Cell><Data ss:Type="String">Restoration of GATA4 expression impedes breast cancer progression by transcriptional repression of ReLA and inhibition of NF-κB signaling</Data></Cell>
    <Cell><Data ss:Type="String">GATA4 is a potential prognostic biomarker and gene therapeutic target for human BrCa</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30187949</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GATA4</Data></Cell>
    <Cell><Data ss:Type="String">Restoration of GATA4 expression impedes breast cancer progression by transcriptional repression of ReLA and inhibition of NF-κB signaling</Data></Cell>
    <Cell><Data ss:Type="String">GATA4 plays a tumor-suppressive role via repression of NF-κB signaling in BrCa cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30187949</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GATA4</Data></Cell>
    <Cell><Data ss:Type="String">GATA4 is upregulated in nasopharyngeal cancer and facilitates epithelial-mesenchymal transition and metastasis through regulation of?SLUG</Data></Cell>
    <Cell><Data ss:Type="String">GATA4 acts as an oncogene and serves crucial roles in NPC and GATA4 may find a potential application as therapeutic option in NPC</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30542490</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GPBAR1</Data></Cell>
    <Cell><Data ss:Type="String">Deficiency of G-protein-coupled bile acid receptor Gpbar1 (TGR5) enhances chemically induced liver carcinogenesis</Data></Cell>
    <Cell><Data ss:Type="String">TGR5 antagonizes the STAT3 pathway through suppressing STAT3 phosphorylation, its transcription activity, and DNA binding activity, which suggests that TGR5 antagonizes liver tumorigenesis at least in part by inhibiting STAT3 signaling</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22911633</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GPBAR1</Data></Cell>
    <Cell><Data ss:Type="String">Pancreatic acinar cell nuclear factor κB activation because of bile acid exposure is dependent on calcineurin</Data></Cell>
    <Cell><Data ss:Type="String">Acinar cell exposure to bile acids and activation of Gpbar1 cause cell injury mediated by Ca2+?signaling and downstream NF-κB translocation</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23744075</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GPBAR1</Data></Cell>
    <Cell><Data ss:Type="String">TGR5 is essential for bile acid-dependent cholangiocyte proliferation in vivo and in vitro</Data></Cell>
    <Cell><Data ss:Type="String">TGR5 is an important mediator of BA-induced cholangiocyte proliferation in vivo and in vitro. Furthermore, TGR5 protects cholangiocytes from death receptor-mediated apoptosis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26420419</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GPBAR1</Data></Cell>
    <Cell><Data ss:Type="String">Membrane bile acid receptor TGR5 predicts good prognosis in ampullary adenocarcinoma patients with hyperbilirubinemia</Data></Cell>
    <Cell><Data ss:Type="String">TGR5 functions as a tumor-suppressor in patients with ampullary adenocarcinoma and preoperative hyperbilirubinemia</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27510297</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GPBAR1</Data></Cell>
    <Cell><Data ss:Type="String">The deficiency of G-protein-coupled bile acid receptor Gpbar1 (TGR5) enhances chemically-induced liver carcinogenesis</Data></Cell>
    <Cell><Data ss:Type="String">TGR5 antagonizes STAT3 pathway through suppressing STAT3 phosphorylation, its transcription activity and DNA binding activity, which suggests that TGR5 antagonizes liver tumorigenesis at least in part by inhibiting STAT3 signaling</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22911633</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GSTP1</Data></Cell>
    <Cell><Data ss:Type="String">Predictive role of GSTP1-containing exosomes in chemotherapy-resistant breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Affecting drug metabolism&#45;&#45;-Anthracycline/taxane-based neoadjuvant chemotherapy</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">28438694</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GSTP1</Data></Cell>
    <Cell><Data ss:Type="String">Cruciferous vegetables, the GSTP1 Ile105Val genetic polymorphism, and breast cancer risk</Data></Cell>
    <Cell><Data ss:Type="String">Cruciferous vegetable intake consistent with high isothiocyanate exposure may reduce breast cancer risk. Cruciferous vegetable intake also may ameliorate the effects of the GSTP1 genotype</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">18326615</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GSTP1</Data></Cell>
    <Cell><Data ss:Type="String">GSTP1 methylation and polymorphism increase the risk of breast cancer and the effects of diet and lifestyle in breast cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">GSTP1 methylation is a major event in breast carcinogenesis and may act as a tumor-specific biomarker</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23226781</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GSTP1</Data></Cell>
    <Cell><Data ss:Type="String">The GSTP1 105Val Allele Increases Breast Cancer Risk and Aggressiveness but Enhances Response to Cyclophosphamide Chemotherapy in North China</Data></Cell>
    <Cell><Data ss:Type="String">GSTP1 Ile105Val genotype may help screen for high-risk populations and direct individualized therapy</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23826324</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GSTP1</Data></Cell>
    <Cell><Data ss:Type="String">Association of GSTP1 Methylation with Aggressive Phenotype in ER-positive Breast Cancer</Data></Cell>
    <Cell><Data ss:Type="String">GSTP1 methylation may well be associated with the pathogenesis of the biologically-aggressive phenotype in ER-positive breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24324107</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GSTP1</Data></Cell>
    <Cell><Data ss:Type="String">GSTP1 Is a Driver of Triple-Negative Breast Cancer Cell Metabolism and Pathogenicity</Data></Cell>
    <Cell><Data ss:Type="String">GSTP1 inhibitors as a novel therapeutic strategy for combatting TNBCs through impairing key cancer metabolism and signaling pathways</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27185638</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GSTP1</Data></Cell>
    <Cell><Data ss:Type="String">Prognostic significance of GSTP1 in patients with triple negative breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">GSTP1 protein may be a novel prognosis marker for TNBC patients in China</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28978147</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GSTP1</Data></Cell>
    <Cell><Data ss:Type="String">CLDN6 promotes chemoresistance through GSTP1 in human breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">High expression of CLDN6 confers chemoresistance on breast cancer which is mediated by GSTP1, the activity of which is regulated by p53</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29116019</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GTF2I</Data></Cell>
    <Cell><Data ss:Type="String">A specific missense mutation in GTF2I occurs at high frequency in thymic epithelial tumors</Data></Cell>
    <Cell><Data ss:Type="String">GTF2I mutation correlated with better survival. GTF2I β and δ isoforms were expressed in TETs, and both mutant isoforms were able to stimulate cell proliferation in vitro</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24974848</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GTF2I</Data></Cell>
    <Cell><Data ss:Type="String">GTF2I mutation frequently occurs in more indolent thymic epithelial tumors and predicts better prognosis</Data></Cell>
    <Cell><Data ss:Type="String">The frequency of the GTF2I mutation is higher in more indolent TETs, and correlates with better prognosis.  </Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28676218</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GTF2I</Data></Cell>
    <Cell><Data ss:Type="String">GTF2I Mutations Are Common in Thymic Epithelial Tumors But Not in Hematological Malignancies</Data></Cell>
    <Cell><Data ss:Type="String">GTF2I mutation is not present or is uncommon in these diseases</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28982856</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GTF2I</Data></Cell>
    <Cell><Data ss:Type="String">The Integrated Genomic Landscape of Thymic Epithelial Tumors</Data></Cell>
    <Cell><Data ss:Type="String">The Integrated Genomic Landscape of Thymic Epithelial Tumors</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29438696</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">GTF2I</Data></Cell>
    <Cell><Data ss:Type="String">Comprehensive epigenetic analyses reveal master regulators driving lung metastasis of breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">TFAP2C, GTF2I and LMO4 were found to have potential prognostic value for lung metastasis free (LMF) survival of breast cance</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31215771</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HDC</Data></Cell>
    <Cell><Data ss:Type="String">Histamine synthesis and content in benign and malignant breast tumours. Its effects on other host tissues</Data></Cell>
    <Cell><Data ss:Type="String">The HDC-activity of cancerous tissue was significantly higher (P &lt; 0.01) than that registered in the healthy mammary gland tissue of the same patient, being even more pronounced in benign tumour tissue (P &lt; 0.001)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">7952401</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HDC</Data></Cell>
    <Cell><Data ss:Type="String">Concentration of histamine in serum and tissues of the primary ductal breast cancers in women</Data></Cell>
    <Cell><Data ss:Type="String">The activity of HDC was significantly higher in cancerous tissues than in adjacent healthy tissues (54.7+/-17.1 vs. 34.5+/-24.3 pmol/min per mg; P&lt;0.001), but there was no difference in the activity of DAO (14.0+/-6.4 vs. 14.4+/-10.9 pmol/min per mg)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">15927833</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HDC</Data></Cell>
    <Cell><Data ss:Type="String">The Role of Cyclooxygenase-2 in Mediating the Effects of Histamine on Cell Proliferation and Vascular Endothelial Growth Factor Production in Colorectal Cancer</Data></Cell>
    <Cell><Data ss:Type="String">Histidine decarboxylase activity and histamine content were also significantly higher in metastatic tumors than in nonmetastatic ones</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">16203768</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HDC</Data></Cell>
    <Cell><Data ss:Type="String">Metabolism of histamine in tissues of primary ductal breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">A significant increase in the concentration of histamine in plasma (P &lt; .01) and tissues of ductal breast cancers (P &lt; .001), and in the activity of histidine decarboxylase (P &lt; .01), aromatic L-amino acids (P &lt; .05), and histamine methyltransferase (P &lt; .05) was found</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19375125</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HDC</Data></Cell>
    <Cell><Data ss:Type="String">Associations of polymorphisms in histidine decarboxylase, histamine N-methyltransferase and histamine receptor H3 genes with breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Polymorphisms of HDC gene were significantly associated with breast cancer in Chinese Han population and may be novel diagnostic or therapeutic targets for breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24835231</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HER2</Data></Cell>
    <Cell><Data ss:Type="String">Clinical application of a microfluidic chip for immunocapture and quantification of circulating exosomes to assist breast cancer diagnosis and molecular classification</Data></Cell>
    <Cell><Data ss:Type="String">The exosomal HER2 expression levels were almost consistent with that in tumor tissues assessed by immunohistochemical staining</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">28369094</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HER2</Data></Cell>
    <Cell><Data ss:Type="String">The HER2 Receptor in Breast Cancer: Pathophysiology, Clinical Use, and New Advances in Therapy</Data></Cell>
    <Cell><Data ss:Type="String">Human epidermal growth factor receptor 2 (HER2) is overexpressed in around 20-30% of breast cancer tumors</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23320171</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HER2</Data></Cell>
    <Cell><Data ss:Type="String">HER2-targeted therapies -a role beyond breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">HER2 is an established therapeutic target in a large subset of women with breast cancer; a variety of agents including trastuzumab, pertuzumab, lapatinib, neratinib and trastuzumab emtansine (T-DM1) have been approved for the treatment of HER2-positive breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30922362</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HER2</Data></Cell>
    <Cell><Data ss:Type="String">Activating HER2 mutations in HER2 gene amplification negative breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">The majority of HER2 somatic mutations in breast cancer patients are activating mutations that likely drive tumorigenesis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23220880</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HER2</Data></Cell>
    <Cell><Data ss:Type="String">HER2 and responsiveness of breast cancer to adjuvant chemotherapy</Data></Cell>
    <Cell><Data ss:Type="String">Amplification of HER2 in breast-cancer cells is associated with clinical responsiveness to anthracycline-containing chemotherapy</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">16707747</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HER2</Data></Cell>
    <Cell><Data ss:Type="String">Intratumoral heterogeneity of HER2 gene amplification in breast cancer: its clinicopathological significance</Data></Cell>
    <Cell><Data ss:Type="String">Intratumoral heterogeneity of HER2 gene amplification is present in a subset of HER2-amplified breast cancers, especially in cases with low-grade HER2 amplification and equivocal HER2 expression, indicating a need for HER2 testing on more representative, larger tumor samples for accurate assessment of HER2 status in such cases</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22388760</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HER2</Data></Cell>
    <Cell><Data ss:Type="String">HER2-associated radioresistance of breast cancer stem cells isolated from HER2-negative breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">HER2-mediated prosurvival signaling network is responsible for the aggressive phenotype of BCSCs that could be targeted to control the therapy-resistant HER2(-/low) breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23091114</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HER2</Data></Cell>
    <Cell><Data ss:Type="String">HER2 and TOP2A as predictive markers for anthracycline-containing chemotherapy regimens as adjuvant treatment of breast cancer: a meta-analysis of individual patient data.</Data></Cell>
    <Cell><Data ss:Type="String">Although HER2 amplification and combined TOP2A amplification and deletion may have some value in the prediction of responsiveness to anthracycline-based chemotherapy, our findings do not support the use of anthracyclines only in patients with HER2-amplified or TOP2A-aberrated tumours</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21917518</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HEXA</Data></Cell>
    <Cell><Data ss:Type="String">Hypermethylation contributes to down-regulation of lysosomal β-hexosaminidase α subunit in prostate cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">The HEXA promoter region in LNCaP and PC3 cell lines had methylated CpG islands, as confirmed by 5'-Aza-2'-deoxycitidine treatment, in PC3 cells, used as cell cancer model</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24389457</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HLA-DQA1</Data></Cell>
    <Cell><Data ss:Type="String">Contribution of the TP53, OGG1, CHRNA3, and HLA-DQA1 genes to the risk for lung squamous cell carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">Genotypes for two DNA repair genes, TP53 and OGG1, showed significant associations with SQC risk (p &lt; 0.05), and those for two GWAS genes, CHRNA3 and HLA-DQA1, showed significant associations with SQC risk (P &lt; 0.05) with odds ratios between 1.65 (95% confidence interval = 1.06-2.57 for OGG1) and 2.57 (95% confidence interval = 1.03-6.87 for CHRNA3)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21623257</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HLA-DQA1</Data></Cell>
    <Cell><Data ss:Type="String">HLA-DRB1,-DQA1 and -DQB1 allele and haplotype frequencies in female patients with early onset breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">HLA-DQA1*0301 allele is mainly associated with increased risk of breast cancer including early-onset of the disease. HLA-DQA1*0505 and HLA-DRB1*1301 are involved in protection. We conclude that specific alleles of HLA class II influence breast cancer risk</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21720852</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HLA-DQA1</Data></Cell>
    <Cell><Data ss:Type="String">Association between HLA-DQA1, HLA-DQB1 and oral cancer</Data></Cell>
    <Cell><Data ss:Type="String">Both HLA-DQA1* and HLA-DQB1* allele frequencies in oral cancer patients revealed no significant difference from those of control groups</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21943816</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HLA-DQA1</Data></Cell>
    <Cell><Data ss:Type="String">HLA-DQA1 &amp; DQB1 variants associated with hepatitis B virus-related chronic hepatitis, cirrhosis &amp; hepatocellular carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">Our results revealed HLA-DQA1*0101/2/4 - DQA1*0103 - DQB1*0302/3 and DQB1*0601 as protective and DQB1*0402 as risk alleles. The study suggests that various subtypes of HLA-DQA1 and DQB1 are associated with both HBV clearance and development of chronic HBV infections</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30168489</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HLA-DQA1</Data></Cell>
    <Cell><Data ss:Type="String">High expression of HLA-DQA1 predicts poor outcome in patients with esophageal squamous cell carcinoma in Northern China</Data></Cell>
    <Cell><Data ss:Type="String">HLA-DQA1 plays an important role in ESCC progression and may be a biomarker for ESCC diagnosis and prognosis, as well as a potential target for the treatment of patients with ESCC</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30813145</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HOXC6</Data></Cell>
    <Cell><Data ss:Type="String">Exosomes enriched in stemness/metastatic-related mRNAS promote oncogenic potential in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Stemness markers and enhance proliferation,migration and invasion abilities of neighboring cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">26528758</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HOXC6</Data></Cell>
    <Cell><Data ss:Type="String">Bisphenol-A induces expression of HOXC6, an estrogen-regulated homeobox-containing gene associated with breast cancer</Data></Cell>
    <Cell><Data ss:Type="String"> HOXC6, which is a critical player in mammary gland development, is upregulated in multiple cases of breast cancer, and is transcriptionally regulated by E2 and BPA, in vitro and in vivo</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25725483</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HOXC6</Data></Cell>
    <Cell><Data ss:Type="String">The role of HOXC6 in prostate cancer development</Data></Cell>
    <Cell><Data ss:Type="String">HOXC6 is a novel candidate biomarker for PCa not only in early detection but also for monitoring of progression or response to therapy</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26310814</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HOXC6</Data></Cell>
    <Cell><Data ss:Type="String">Identification of activated enhancers and linked transcription factors in breast, prostate, and kidney tumors by tracing enhancer networks using epigenetic traits</Data></Cell>
    <Cell><Data ss:Type="String">HOXC6 and DLX1 are associated with different clusters of prostate tumor-specific enhancers and confer distinct transcriptomic changes upon knockdown in C42B prostate cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27833659</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HOXC6</Data></Cell>
    <Cell><Data ss:Type="String">Long noncoding RNA Linc00339 promotes triple-negative breast cancer progression through miR-77-p/HOXC6 signaling pathway</Data></Cell>
    <Cell><Data ss:Type="String">Linc00339/miR-377-3p/HOXC6 axis played a critical role in TNBC progression and might be a promising therapeutic target for TNBC treatment</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30618083</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HOXC6</Data></Cell>
    <Cell><Data ss:Type="String">Overexpression of HOXC6 promotes cell proliferation and migration via MAPK signaling and predicts a poor prognosis in glioblastoma</Data></Cell>
    <Cell><Data ss:Type="String">HOXC6 promoted proliferation and migration of GBM cells via the activation of MAPK pathway</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31564976</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HRNR</Data></Cell>
    <Cell><Data ss:Type="String">Hornerin promotes tumor progression and is associated with poor prognosis in hepatocellular carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">HRNR promotes tumor progression and is correlated with a poor HCC prognosis. HRNR may contribute to HCC progression via the regulation of the AKT pathway.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30103712</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HRNR</Data></Cell>
    <Cell><Data ss:Type="String">Hornerin promotes tumor progression and is associated with poor prognosis in hepatocellular carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">The knockdown of HRNR by shRNAs significantly inhibited the proliferation, colony formation, migration and invasion of HCC tumor cells. HRNR silencing led to the decreased phosphorylation of AKT signaling.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30103712</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-let-7a</Data></Cell>
    <Cell><Data ss:Type="String">Plasma exosome microRNAs are indicative of breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Based on the selective enrichment and absolute abundance, we identified miR-1246, miR-122, miR-21, and let-7a as candidate exosome microRNAs that may serve as biomarkers indicative of breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">27608715</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-let-7a</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA let-7a suppresses breast cancer cell migration and invasion through downregulation of C-C chemokine receptor type 7</Data></Cell>
    <Cell><Data ss:Type="String">Targeting of CCL21-CCR7 signaling is a valid approach for breast cancer therapy and that let-7a directly binds to the 3'UTR of CCR7 and blocks its protein expression, thereby suppressing migration and invasion of human breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22251626</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-let-7a</Data></Cell>
    <Cell><Data ss:Type="String">Let-7a inhibits growth and migration of breast cancer cells by targeting HMGA1</Data></Cell>
    <Cell><Data ss:Type="String">Let-7a plays an important role as a tumor suppressor gene by targeting HMGA1, which may open novel perspectives for clinical treatments against breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25846193</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-let-7a</Data></Cell>
    <Cell><Data ss:Type="String">Expression of tumor suppressors miR-195 and let-7a as potential biomarkers of invasive breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-195 and let-7a can be used as a non-invasive biomarker for breast cancer detection</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29995098</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-let-7a</Data></Cell>
    <Cell><Data ss:Type="String">Role of let-7 family microRNA in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">This article will provide the in-depth insight into the biology of let-7 miRNA and its role in the breast cancer progression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30159414</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-let-7a</Data></Cell>
    <Cell><Data ss:Type="String">Plasma miR-21, miR-155, miR-10b, and Let-7a as the potential biomarkers for the monitoring of breast cancer patient</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-let-7a might be considered as a respectable diagnostic tool for monitoring of breast cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30568292</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-let-7a</Data></Cell>
    <Cell><Data ss:Type="String">Robust expression of tumor suppressor miRNA- let-7 and miR-195 detected in plasma of Saudi female breast cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">In order to facilitate earlier detection of breast cancer, blood based screening of hsa-miR-195 and let-7 may be beneficial in a female patient cohort</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29183284</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-100</Data></Cell>
    <Cell><Data ss:Type="String">Exosomes from Drug-Resistant Breast Cancer Cells Transmit Chemoresistance by a Horizontal Transfer of MicroRNAs</Data></Cell>
    <Cell><Data ss:Type="String">Target gene prediction and pathway analysis showed the involvement of miR-100, miR-222, and miR-30a in pathways implicated in cancer pathogenesis, membrane vesiculation and therapy failure.The transmition of chemoresistance by a horizontal transfer of miRNAs</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">24740415</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-100</Data></Cell>
    <Cell><Data ss:Type="String">EphB6 receptor modulates micro RNA profile of breast carcinoma cells</Data></Cell>
    <Cell><Data ss:Type="String">MiR-100 and  EphB6 involve in PI3K/Akt/mTOR pathways which is capable of initiating signal transduction from the cell surface to the nucleus resulting in the altered expression of a variety of genes involved in tumorigenesis and invasion</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21811619</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-100</Data></Cell>
    <Cell><Data ss:Type="String">miR-100 suppresses IGF2 and inhibits breast tumorigenesis by interfering with proliferation and survival signaling</Data></Cell>
    <Cell><Data ss:Type="String">MiR-100 as a context-dependent master regulator of the IGF/mTOR pathway and a potential target for therapeutic approaches</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22926517</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-100</Data></Cell>
    <Cell><Data ss:Type="String">By promoting cell differentiation, miR-100 sensitizes basal-like breast cancer stem cells to hormonal therapy</Data></Cell>
    <Cell><Data ss:Type="String">MiR-100 is a negative prognostic factor and is associated with gene signatures of high grade undifferentiated tumors</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25537513</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-100</Data></Cell>
    <Cell><Data ss:Type="String">The role of miR-100 in regulating apoptosis of breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">Antagonism of miR-100 in SK-BR-3 cells increased the expression of MTMR3, a target gene of miR-100, which resulted in the activation of p27 and eventually led to G2/M cell-cycle arrest and apoptosi</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26130569</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-101</Data></Cell>
    <Cell><Data ss:Type="String">Increased serum levels of circulating exosomal microRNA-373 in receptor-negative breast cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">In conclusion, our findings suggest cell-free miR-101 and miR-373 as breast cancer-specific markers</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">25333260</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-101</Data></Cell>
    <Cell><Data ss:Type="String">miR-101 promotes breast cancer cell apoptosis by targeting Janus kinase 2</Data></Cell>
    <Cell><Data ss:Type="String">MiR-101 suppressed proliferation and promoted apoptosis in breast cancer cells by targeting Jak2. These findings indicate that manipulation of miR-101 expression may represent a novel therapeutic strategy in the treatment of breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25059472</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-101</Data></Cell>
    <Cell><Data ss:Type="String">MiRNA-101 inhibits breast cancer growth and metastasis by targeting CX chemokine receptor 7</Data></Cell>
    <Cell><Data ss:Type="String">STAT3 signaling downstream of CXCR7 is involved in miR-101 regulation of breast cancer cell behaviors. These findings have implications for the potential application of miR-101 in breast cancer treatment</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26360780</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-101</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-101 Inhibits Growth, Proliferation and Migration and Induces Apoptosis of Breast Cancer Cells by Targeting Sex-Determining Region Y-Box 2</Data></Cell>
    <Cell><Data ss:Type="String">SOX2 knockdown mimicked the effects of miR-101 overexpression on the malignant behaviors of BC cells, while SOX2 overexpression mitigated the miR-101-induced inhibition of these effects;miR-101 plays a critical role in suppressing tumor progression by directly targeting SOX2</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28946143</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-101</Data></Cell>
    <Cell><Data ss:Type="String">MiR-101 may be a novel marker for diagnosis and prognosis in breast cancer, which might improve the clinical outcomes of patients with breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-101 is a novel biomarker for diagnosis and prognosis in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-103</Data></Cell>
    <Cell><Data ss:Type="String">Blood Circulating Exosomes Contain Distinguishable Fractions of Free and Cell-Surface-Associated Vesicles</Data></Cell>
    <Cell><Data ss:Type="String">Preliminary data indicated that detection of cancer-specific miRNA (miR-103, miR-191, miR-195) in exosomes associated with the fraction of red blood cells allowed to discriminate HFs and BCPs more precisely compared to cell-free exosomes circulating in plasma</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">30868953</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-103</Data></Cell>
    <Cell><Data ss:Type="String">A MicroRNA targeting dicer for metastasis control</Data></Cell>
    <Cell><Data ss:Type="String">In human primary breast tumors, miR-103/107, but not Dicer mRNA, as prognostic marker. miR-103/107 with a better patient stratification capacity than Dicer transcripts.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">20603000</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-103</Data></Cell>
    <Cell><Data ss:Type="String">A MicroRNA targeting dicer for metastasis control</Data></Cell>
    <Cell><Data ss:Type="String">In metastatic cells, high levels of miR-103/107 attenuate Dicer expression: this empowers invasive and metastatic properties without major impact on primary tumor growth.At the cellular level, a key event fostered by miR-103/107 is induction of epithelial-to-mesenchymal transition (EMT), attained by downregulating miR-200 levels.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">20603000</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-103</Data></Cell>
    <Cell><Data ss:Type="String">Upregulation of serum miR-103 predicts unfavorable prognosis in patients with colorectal cancer.</Data></Cell>
    <Cell><Data ss:Type="String">Serum miR-103 was significantly correlated with worse clinical factors, as well as poorer recurrence-free survival or overall survival. Finally, multivariate analysis confirmed that serum miR-103 was an independent prognostic marker for CRC.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30058684</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-105</Data></Cell>
    <Cell><Data ss:Type="String">Cancer-secreted hsa-miR-105 destroys vascular endothelial barriers to promote metastasis</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-105 has significantly up-regulated and has been extensively implicated in cancer progression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">24735924</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-105</Data></Cell>
    <Cell><Data ss:Type="String">Exosomal miRNA profile as complementary tool in the diagnostic and prediction of treatment response in localized breast cancer under neoadjuvant chemotherapy</Data></Cell>
    <Cell><Data ss:Type="String">Higher levels of exosomal miRNA-21, miRNA-222, and miRNA-155 were significantly associated with the presence of circulating tumor cells;Liquid biopsies based on exosomal miRNAs and circulating tumor cells can be a complementary clinical tool for improving breast cancer diagnosis and prognosis</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">30728048</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-105</Data></Cell>
    <Cell><Data ss:Type="String">Cancer-secreted miR-105 destroys vascular endothelial barriers to promote metastasis</Data></Cell>
    <Cell><Data ss:Type="String">MiR-105 can be detected in the circulation at the pre-metastatic stage, and its levels in the blood and tumor are associated with ZO-1 expression and metastatic progression in early-stage breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24735924</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-105</Data></Cell>
    <Cell><Data ss:Type="String">miR-105/93-3p promotes chemoresistance and circulating miR-105/93-3p acts as a diagnostic biomarker for triple negative breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-105/93-3p levels represent a prime candidate for development into a diagnostic biomarker for both early- and late-stage TNBC</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29258605</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-105</Data></Cell>
    <Cell><Data ss:Type="String">Cancer-cell-secreted exosomal miR-105 promotes tumour growth through the MYC-dependent metabolic reprogramming of stromal cells</Data></Cell>
    <Cell><Data ss:Type="String">MiR-105-mediated metabolic reprogramming of stromal cells contributes to sustained tumour growth by conditioning the shared metabolic environment</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29662176</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-105</Data></Cell>
    <Cell><Data ss:Type="String">miR-195/miR-497 Regulate CD274 Expression of Immune Regulatory Ligands in Triple-Negative Breast Cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-105, and miR-340 expression levels were associated with a poor prognosis in patients with breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30607158</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-105</Data></Cell>
    <Cell><Data ss:Type="String">The Diverse Oncogenic and Tumor Suppressor Roles of microRNA-105 in Cancer</Data></Cell>
    <Cell><Data ss:Type="String">This review may provide new ideas for applying miR-105 as a diagnostic and prognostic biomarker</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31281797</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-105</Data></Cell>
    <Cell><Data ss:Type="String">The Diverse Oncogenic and Tumor Suppressor Roles of microRNA-105 in Cancer</Data></Cell>
    <Cell><Data ss:Type="String">We emphasize the characteristics of miR-105 in cancer to elucidate various deadly tumors and discuss transcriptional regulations that may explain fluctuations in miR-105 expression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31281797</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-106b</Data></Cell>
    <Cell><Data ss:Type="String">Molecular characterization of exosome-like vesicles from breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">The mir-106b is found in higher levels in MCF-Eox as well, which can promote breast cancer invasion and metastasis by targeting BRMS1 and RB</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">24468161</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-106b</Data></Cell>
    <Cell><Data ss:Type="String">The miR-106b-25 cluster targets Smad7, activates TGF-β signaling, and induces EMT and tumor initiating cell characteristics downstream of Six1 in human breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-106b-25 may provide a novel molecular explanation, through the Six1 regulated miR-106b-25 cluster, by which TGF-β signaling shifts from tumor suppressive to tumor promoting</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22286770</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-106b</Data></Cell>
    <Cell><Data ss:Type="String">Downregulation of miR-106b induced breast cancer cell invasion and motility in association with overexpression of matrix metalloproteinase 2</Data></Cell>
    <Cell><Data ss:Type="String">MMP2 upregulation plays an important role in BC bone metastasis through ERK pathways, and miR-106b directly regulates MMP2 expression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24164962</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-106b</Data></Cell>
    <Cell><Data ss:Type="String">Prognostic value of miR-106b expression in breast cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">MiR-106b was found to be associated with a high risk of recurrence of breast cancer, and miR-106b is a putative plasma marker for risk assessment in patients with breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25619461</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-10a</Data></Cell>
    <Cell><Data ss:Type="String">Cancer Exosomes Perform Cell-Independent MicroRNA Biogenesis and Promote Tumorigenesis</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-10a has significantly up-regulated and has been extensively implicated in cancer progression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">25446899</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-10a</Data></Cell>
    <Cell><Data ss:Type="String">Increased expression of miR-126 and miR-10a predict prolonged relapse-free time of primary oestrogen receptor-positive breast cancer following tamoxifen treatment</Data></Cell>
    <Cell><Data ss:Type="String">MiR-126 and miR-10a are independent predictors for tumour relapse in early postmenopausal breast cancer patients treated with adjuvant tamoxifen.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23968733</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-10a</Data></Cell>
    <Cell><Data ss:Type="String">The prognostic significance of RUNX2 and miR-10a/10b and their inter-relationship in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Higher expression of RUNX2 and miR-10a/b was associated with adverse outcome of breast cancer. Expression levels of RUNX2 and miR-10a/b individually or jointly are potential prognostic factors for predicting breast cancer recurrence.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25266482</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-10a</Data></Cell>
    <Cell><Data ss:Type="String">miR-10a suppresses colorectal cancer metastasis by modulating the epithelial-to-mesenchymal transition and anoikis</Data></Cell>
    <Cell><Data ss:Type="String">Higher miR-10a levels are significantly correlated with less aggressive CRC phenotypes in patients, which may have prognostic and therapeutic value for CRC patients in the future.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28383561</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-10a</Data></Cell>
    <Cell><Data ss:Type="String">miR-10a suppresses colorectal cancer metastasis by modulating the epithelial-to-mesenchymal transition and anoikis</Data></Cell>
    <Cell><Data ss:Type="String">MiR-10a promoted migration and invasion in vitro but inhibited metastasis in vivo by regulating the epithelial-to-mesenchymal transition and anoikis.Furthermore, matrix metalloproteinase 14 (MMP14) and actin gamma 1 (ACTG1) were validated as target genes of miR-10a in CRC cells.Ectopic expression of MMP14 and ACTG1 counteracted the decreased cell adhesion and anoikis resistance activities induced by miR-10a.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28383561</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-10b</Data></Cell>
    <Cell><Data ss:Type="String">Cancer Exosomes Perform Cell-Independent MicroRNA Biogenesis and Promote Tumorigenesis</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-10b has significantly up-regulated and has been extensively implicated in cancer progression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">25446899</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-10b</Data></Cell>
    <Cell><Data ss:Type="String">Exosome-mediated transfer of hsa-miR-10b promotes cell invasion in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-10b secretes protein levels that inhibit its target genes such as HOXD10 and KLF4 and induces invasion of breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">25428807</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-10b</Data></Cell>
    <Cell><Data ss:Type="String">Tumour invasion and metastasis initiated by microRNA-10b in breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-10b (miR-10b) is highly expressed in metastatic breast cancer cells and positively regulates cell migration and invasion.Overexpression of miR-10b in otherwise non-metastatic breast tumours initiates robust invasion and metastasis. The level of miR-10b expression in primary breast carcinomas correlates with clinical progression.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">17898713</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-10b</Data></Cell>
    <Cell><Data ss:Type="String">Tumour invasion and metastasis initiated by microRNA-10b in breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">Expression of miR-10b is induced by the transcription factor Twist, which binds directly to the putative promoter of mir-10b (MIRN10B). The miR-10b induced by Twist proceeds to inhibit translation of the messenger RNA encoding homeobox D10, resulting in increased expression of a well-characterized pro-metastatic gene, RHOC.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">17898713</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-10b</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-10b is overexpressed in malignant glioma and associated with tumor invasive factors, uPAR and RhoC.</Data></Cell>
    <Cell><Data ss:Type="String">MiR-10b might play some role in the invasion of glioma cells.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19536818</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-10b</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-10b is overexpressed in malignant glioma and associated with tumor invasive factors, uPAR and RhoC.</Data></Cell>
    <Cell><Data ss:Type="String">MiR-10b expression pattern in glioma. miR-10b inhibits the translation of mRNA encoding HOXD10, which modulates many genes that promote invasion, migration, extracellular matrix remodeling and tumor progression, including uPAR, RhoC, α3 integrin, β integrin and matrix metalloprotease-4 (MMP-4).</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19536818</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-10b</Data></Cell>
    <Cell><Data ss:Type="String">The level of circulating miRNA-10b and miRNA-373 in detecting lymph node metastasis of breast cancer: potential biomarkers.</Data></Cell>
    <Cell><Data ss:Type="String">Circulating miRNA-10b and miRNA-373 are potential biomarkers for detecting the lymph node status of breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23238818</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1207-5p</Data></Cell>
    <Cell><Data ss:Type="String">miR-1207-5p and miR-1266 suppress gastric cancer growth and invasion by targeting telomerase reverse transcriptase</Data></Cell>
    <Cell><Data ss:Type="String">MiR-1207-5p and miR-1266 were determined to be hTERT suppressors in gastric cancer, and the delivery of these two miRNAs represents a novel therapeutic strategy for gastric cancer treatment</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24481448</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1207-5p</Data></Cell>
    <Cell><Data ss:Type="String">miR-1207-5p suppresses lung cancer growth and metastasis by targeting CSF1</Data></Cell>
    <Cell><Data ss:Type="String">MiR-1207-5p-CSF1 axis maybe a new regulator of lung cancer development through modulating the tumor microenvironment</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27107415</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1207-5p</Data></Cell>
    <Cell><Data ss:Type="String">PVT1-derived miR-1207-5p promotes breast cancer cell growth by targeting STAT6</Data></Cell>
    <Cell><Data ss:Type="String">PVT1-derived miR-1207-5p promotes the proliferation of breast cancer cells by targeting STAT6, which in turn controls CDKN1A and CDKN1B expression;miR-1207-5p might be a potential target for breast cancer therapy</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28235236</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1207-5p</Data></Cell>
    <Cell><Data ss:Type="String">miR-1207-5p regulates the sensitivity of triple-negative breast cancer cells to Taxol treatment via the suppression of LZTS1 expression</Data></Cell>
    <Cell><Data ss:Type="String">There was a notable elevation in the expression of miR-1207-5p and a reduction in the expression of LZTS1 in the Taxol non-responsive TNBC tissues when compared with the Taxol-responsive TNBC tissues</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30655858</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1207-5p</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA miR-1207-5p-repression of ATRA receptors determine retinoid-resistance in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-1207-5p in the regulation of retinoid-resistance in the BLBC cells and reflects on potential use of a combination of miR-1207-5p antagonists (antagomir and sponges) and ATRA as potent chemotherapy against hard-to-cure BLBC</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-122</Data></Cell>
    <Cell><Data ss:Type="String">Breast-cancer-secreted hsa-miR-122 reprograms glucose metabolism in premetastatic niche to promote metastasis</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-122 suppresses glucose uptake by downregulating the glycolytic enzyme pyruvate kinase (PKM)to promote metastasis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">25621950</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-122</Data></Cell>
    <Cell><Data ss:Type="String">Plasma exosome microRNAs are indicative of breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Based on the selective enrichment and absolute abundance, we identified miR-1246, miR-122, miR-21, and let-7a as candidate exosome microRNAs that may serve as biomarkers indicative of breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">27608715</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-122</Data></Cell>
    <Cell><Data ss:Type="String">De novo sequencing of circulating miRNAs identifies novel markers predicting clinical outcome of locally advanced breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Certain miRNAs can serve as potential blood-based biomarkers for NCT response, and that miR-122 prevalence in the circulation predicts BC metastasis in early-stage patients</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22400902</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-122</Data></Cell>
    <Cell><Data ss:Type="String">MiR-122 inhibits cell proliferation and tumorigenesis of breast cancer by targeting IGF1R</Data></Cell>
    <Cell><Data ss:Type="String">MiR-122 may serve as a novel therapeutic or diagnostic/prognostic-target for treating BC</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23056576</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-122</Data></Cell>
    <Cell><Data ss:Type="String">MiR-122 inhibits cell proliferation and tumorigenesis of breast cancer by targeting IGF1R</Data></Cell>
    <Cell><Data ss:Type="String">MiR-122 functions as a tumor suppressor and plays an important role in inhibiting the tumorigenesis through targeting IGF1R and regulating PI3K/Akt/mTOR/p70S6K pathway</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23056576</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-122</Data></Cell>
    <Cell><Data ss:Type="String">Breast-cancer-secreted miR-122 reprograms glucose metabolism in premetastatic niche to promote metastasis</Data></Cell>
    <Cell><Data ss:Type="String">By modifying glucose utilization by recipient premetastatic niche cells, cancer-derived extracellular miR-122 is able to reprogram systemic energy metabolism to facilitate disease progression</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25621950</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-122</Data></Cell>
    <Cell><Data ss:Type="String">Evaluation of miR-122 as a Serum Biomarker for Hepatotoxicity in Investigative Rat Toxicology Studies</Data></Cell>
    <Cell><Data ss:Type="String">Serum miR-122 levels can be utilized as a biomarker of hepatotoxicity in acute and subacute rat toxicology studies, and its performance can rival or exceed those of standard enzyme biomarkers such as the liver transaminases</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26123229</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-122</Data></Cell>
    <Cell><Data ss:Type="String">Inhibition of breast cancer cell proliferation and tumorigenesis by long non-coding RNA RPPH1 down-regulation of miR-122 expression</Data></Cell>
    <Cell><Data ss:Type="String">Breast cancer progression can be promoted by directly targeting miR-122 through lncRNA RPPH1</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29200969</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1228-5p</Data></Cell>
    <Cell><Data ss:Type="String">A Serum MicroRNA Panel as Potential Biomarkers for Hepatocellular Carcinoma Related with Hepatitis B Virus</Data></Cell>
    <Cell><Data ss:Type="String">Tan and colleagues identified a serum of miRNA panel (hsa-miR-206, hsa-miR-141-3p, hsa-miR-433-3p, hsa-miR-1228-5p, hsa-miR-199a-5p, hsa-miR-122-5p, hsa-miR-192-5p, and hsa-miR-26a-5p) that has considerable clinical value in HCC diagnosis</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25238238</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1233-5p</Data></Cell>
    <Cell><Data ss:Type="String">Significance of microRNA-based biomarkers for pancreatic cancer</Data></Cell>
    <Cell><Data ss:Type="String">Fifteen miRNAs (miR-106b-3p, miR-1233*, miR-1271-5p, miR-1285-3p, miR-15b-3p*, miR-181c-5p, miR-26b-3p, miR-30d-3p, miR-335-3p*, miR-454-5p*, miR-589-3p, miR-616-3p, miR-663b, miR-664-3p, and miR-744-3p) were significantly dysregulated in patients with PC compared to HC on normalization to both U6 and miR-16</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26605323</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-124-3p</Data></Cell>
    <Cell><Data ss:Type="String">Differential expression of exosomal miRNAs between breast cancer patients with and without recurrence</Data></Cell>
    <Cell><Data ss:Type="String">Of 384 miRNAs, three miRNAs (miR-338-3p, miR-340-5p, and miR-124-3p) were significantly upregulated and eight (miR-29b-3p, miR-20b-5p, miR-17-5p, miR-130a-3p, miR-18a-5p, miR-195-5p, miR-486-5p, and miR-93-5p) were significantly downregulated in the patients with recurrence</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29050253</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-124-3p</Data></Cell>
    <Cell><Data ss:Type="String">Decreased miR-124-3p Expression Prompted Breast Cancer Cell Progression Mainly by Targeting Beclin-1</Data></Cell>
    <Cell><Data ss:Type="String">Decreased miR-124-3p expression prompted breast cancer cell progression mainly by enhancing the expression of autophagy related protein, Beclin-1</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27468577</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-124-3p</Data></Cell>
    <Cell><Data ss:Type="String">miR-124-3p functions as a tumor suppressor in breast cancer by targeting CBL</Data></Cell>
    <Cell><Data ss:Type="String">MiR-124-3p and CBL regulate the proliferation and invasion of breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27842510</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-124-3p</Data></Cell>
    <Cell><Data ss:Type="String">miR-124-3p acts as a potential marker and suppresses tumor growth in gastric cancer</Data></Cell>
    <Cell><Data ss:Type="String">The underlying mechanism for the regulation of gastric cancer by miR-124-3p via targeting of Rac1 and SP1</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30013778</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-124-3p</Data></Cell>
    <Cell><Data ss:Type="String">miR-124-3p could be used as biomarkers for HNSCC diagnosis in the high altitude mestizo Ecuadorian population</Data></Cell>
    <Cell><Data ss:Type="String">Salivary MicroRNAs for Early Detection of Head and Neck Squamous Cell Carcinoma: A Case-Control Study in the High Altitude Mestizo Ecuadorian Population</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30584540</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1246</Data></Cell>
    <Cell><Data ss:Type="String">Exosomal MicroRNA hsa-miR-1246 Promotes Cell Proliferation,Invasion and Drug Resistance by Targeting CCNG2 in Breast Cancer</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-1246 promotes cell proliferation,invasion and drug resistance by targeting CCNG2 in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29216623</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1246</Data></Cell>
    <Cell><Data ss:Type="String">Plasma exosome microRNAs are indicative of breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Based on the selective enrichment and absolute abundance, we identified miR-1246, miR-122, miR-21, and let-7a as candidate exosome microRNAs that may serve as biomarkers indicative of breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">27608715</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1246</Data></Cell>
    <Cell><Data ss:Type="String">Selective release of microRNA species from normal and malignant mammary epithelial cells</Data></Cell>
    <Cell><Data ss:Type="String">MiR-1246 were also reported as valuable potential biomarkers of breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">20976003</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1246</Data></Cell>
    <Cell><Data ss:Type="String">MiR-1246 promotes SiHa cervical cancer cell proliferation, invasion, and migration through suppression of its target gene thrombospondin 2</Data></Cell>
    <Cell><Data ss:Type="String">MiR-1246 might promote CSCC tumorigenesis and progression by the suppression of its target gene THBS2</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24806621</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1246</Data></Cell>
    <Cell><Data ss:Type="String">Novel combination of serum microRNA for detecting breast cancer in the early stage</Data></Cell>
    <Cell><Data ss:Type="String">Combination of five miRNA (miR-246, miR-307-p, miR-634, miR-861-p and miR-875-p) was found to be able to detect breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26749252</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1246</Data></Cell>
    <Cell><Data ss:Type="String">Extracellular miR-1246 promotes lung cancer cell proliferation and enhances radioresistance by directly targeting DR5</Data></Cell>
    <Cell><Data ss:Type="String">MiR-1246 could act as a signaling messenger between irradiated and non-irradiated cells, more importantly, it contributes to cell radioresistance by directly suppressing the DR5 gene</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27129166</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1246</Data></Cell>
    <Cell><Data ss:Type="String">Serum expression levels of microRNA-382-3p, -598-3p, -1246 and -184 in breast cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">MiR-382-3p, -598-3p, -1246 and -184 are all involved in the development of breast cancer, and are promising biomarkers for breast cancer detection</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27347136</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1246</Data></Cell>
    <Cell><Data ss:Type="String">miRNA-1246 induces pro-inflammatory responses in mesenchymal stem/stromal cells by regulating PKA and PP2A</Data></Cell>
    <Cell><Data ss:Type="String">MiR-1246 led to a p65-dependent increase in transcription and release of pro-inflammatory mediators IL-6, CCL2 and CCL5 in MSCs, and increased NF-κB activity and promote inflammatory by direct targeting of the tumor-suppressors PRKAR1A and PPP2CB</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28159925</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1246</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-1246 inhibits cell invasion and epithelial mesenchymal transition process by targeting CXCR4 in lung cancer cells.</Data></Cell>
    <Cell><Data ss:Type="String">miR-1246 inhibited cell invasion and EMT process by targeting CXCR4 and blocking JAK/STAT and PI3K/AKT signal pathways in lung cancer cells.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29171984</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1246</Data></Cell>
    <Cell><Data ss:Type="String">MiR-1246 Promotes Metastasis and Invasion of A549 cells by Targeting GSK-3β Mediated Wnt/β-Catenin Pathway</Data></Cell>
    <Cell><Data ss:Type="String">miR-1246 regulates Wnt/β-catenin pathway through targeting GSK-3β/β-catenin, which partly contributing to tumor metastasis.MiR-1246 may play an essential role in the diagnosis and therapeutic of lung cancer.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30913872</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1246</Data></Cell>
    <Cell><Data ss:Type="String">microRNA-1246 Is an Exosomal Biomarker for Aggressive Prostate Cancer</Data></Cell>
    <Cell><Data ss:Type="String">Ex-miR-1246 expression correlated with increasing pathologic grade, positive metastasis, and poor prognosis</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29437039</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1246</Data></Cell>
    <Cell><Data ss:Type="String">microRNA-1246 Is an Exosomal Biomarker for Aggressive Prostate Cancer</Data></Cell>
    <Cell><Data ss:Type="String">Overexpression of miR-1246 in a prostate cancer cell line significantly inhibited xenograft tumor growth in vivo and increased apoptosis and decreased proliferation, invasiveness, and migration in vitro miR-1246 inhibited N-cadherin and vimentin activities, thereby inhibiting epithelial-mesenchymal transition</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29437039</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1246</Data></Cell>
    <Cell><Data ss:Type="String">Exosome-packaged miR-1246 contributes to bystander DNA damage by targeting LIG4.</Data></Cell>
    <Cell><Data ss:Type="String">MiR-1246 packaged in exosomes could act as a transfer messenger and contribute to DNA damage by directly repressing the LIG4 gene</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30038324</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1246</Data></Cell>
    <Cell><Data ss:Type="String">In Situ Detection of Plasma Exosomal MicroRNA-1246 for Breast Cancer Diagnostics by a Au Nanoflare Probe</Data></Cell>
    <Cell><Data ss:Type="String">Using plasma miR-1246 level detected by our assay as a marker, we differentiated 46 breast cancer patients from 28 healthy controls with 100% sensitivity and 92.9% specificity at the best cutoff</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30350935</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1268a</Data></Cell>
    <Cell><Data ss:Type="String">Polymorphisms in the precursor microRNAs and aflatoxin B1-related hepatocellular carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">Polymorphisms in pre-miRNAs, such as rs28599926 in miR-1268a, can be used as biomarkers for AFB1-related HCC</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26152337</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1268a</Data></Cell>
    <Cell><Data ss:Type="String">Prognostic significance of miR-1268a expression and its beneficial effects for post-operative adjuvant transarterial chemoembolization in hepatocellular carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-1268a may be an independent prognostic factor for HCC patients, and that decreasing microRNA-1268a expression may be beneficial for post-operative adjuvant TACE treatment in HCC</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27796321</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1268a</Data></Cell>
    <Cell><Data ss:Type="String">miR-1268a regulates ABCC1 expression to mediate temozolomide resistance in glioblastoma</Data></Cell>
    <Cell><Data ss:Type="String">MiR-1268a and elucidated its role in modulating TMZ-resistance of GBM cells by targeting ABCC1</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29876787</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1268a</Data></Cell>
    <Cell><Data ss:Type="String">Distinct shed microvesicle and exosome microRNA signatures reveal diagnostic markers for colorectal cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-1268a was specifically enriched in SW480-Exos and miR-107 was enriched in only SW480-CL released EVs</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30608951</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1268a</Data></Cell>
    <Cell><Data ss:Type="String">The microRNA-1268a rs28599926 polymorphism modified diffusely infiltrating astrocytoma risk and prognosis</Data></Cell>
    <Cell><Data ss:Type="String">MiR-1268a rs28599926 polymorphism may be associated with DIA risk and prognosis</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-128</Data></Cell>
    <Cell><Data ss:Type="String">Shikonin Inhibits the Proliferation of Human Breast Cancer Cells by Reducing Tumor-Derived Exosomes</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-128 negatively regulates the level of Bax in MCF7recipient cells and inhibits cell proliferation</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">27322220</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-128</Data></Cell>
    <Cell><Data ss:Type="String">Reduced miR-128 in breast tumor-initiating cells induces chemotherapeutic resistance via Bmi-1 and ABCC5</Data></Cell>
    <Cell><Data ss:Type="String">Reduction in miR-128 leading to Bmi-1 and ABCC5 overexpression is a stem cell-like feature of BT-ICs, which contributes to chemotherapeutic resistance in breast cancers. Ectopic expression of miR-128 sensitizes BT-ICs to the proapoptotic and DNA-damaging effects of doxorubicin, indicating therapeutic potential</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21953503</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-128</Data></Cell>
    <Cell><Data ss:Type="String">Loss of SNAIL regulated miR-128-2 on chromosome 3p22.3 targets multiple stem cell factors to promote transformation of mammary epithelial cells</Data></Cell>
    <Cell><Data ss:Type="String">In summary, we have identified a novel TGF-β/SNAIL/miR-128 axis that provides a new avenue to understand the basis for oncogenic transformation of mammary epithelial cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23019226</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-128</Data></Cell>
    <Cell><Data ss:Type="String">miR-128 and its target genes in tumorigenesis and metastasis</Data></Cell>
    <Cell><Data ss:Type="String">Aberrant expression of miR-128 has been detected in many types of human tumors and its validated target genes are involved in cancer-related biological processes such as cell proliferation, differentiation and apoptosis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23958464</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-128</Data></Cell>
    <Cell><Data ss:Type="String">miR-128 and miR-149 enhance the chemosensitivity of temozolomide by Rap1B-mediated cytoskeletal remodeling in glioblastoma</Data></Cell>
    <Cell><Data ss:Type="String">The expression of miR-128 and miR-149 was downregulated in glioblastoma, and their overexpression inhibited the invasion of glioblastoma cells by targeting Rap1B-mediated cytoskeletal and related molecular alterations</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25017996</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-128</Data></Cell>
    <Cell><Data ss:Type="String">MiR-128 regulation of glucose metabolism and cell proliferation in triple-negative breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-128 might be a prognostic marker and possible molecular target for therapy in patients with TNBC</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29116653</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-128</Data></Cell>
    <Cell><Data ss:Type="String">MiR-128 regulation of glucose metabolism and cell proliferation in triple-negative breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-128 targeting inhibition of the insulin receptor and insulin receptor substrate 1</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29116653</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-130a</Data></Cell>
    <Cell><Data ss:Type="String">Molecular characterization of exosome-like vesicles from breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">Comparing the miRNAs in MDA-Exo to MCF-Exo showed a higher expression of tumorigenic mir-130a in MDA-Exo. it has been shown that mir-130a contribute to tumorigenesis of colon cancer by regulating TGB-尾/Smad signaling</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">24468161</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-130a</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-130a inhibits cell proliferation, invasion and migration in human breast cancer by targeting the RAB5A</Data></Cell>
    <Cell><Data ss:Type="String">MiR-130a is an important tumor suppressor in breast cancer, and imply that miR-130a/RAB5A axis have potential as therapeutic targets for breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25755726</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-130a</Data></Cell>
    <Cell><Data ss:Type="String">MiR-130a and MiR-374a Function as Novel Regulators of Cisplatin Resistance in Human Ovarian Cancer A2780 Cells</Data></Cell>
    <Cell><Data ss:Type="String">The deregulation of miR-374a and miR-130a may be involved in the development and regulation of cisplatin resistance in ovarian cancer cells; miR-130a may be achieved by regulating the MDR1 and PTEN gene expression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26043084</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-130a</Data></Cell>
    <Cell><Data ss:Type="String">miR-130a Deregulates PTEN and Stimulates Tumor Growth</Data></Cell>
    <Cell><Data ss:Type="String">MiR-130a overexpression in human breast cancer cells promoted Akt phosphorylation, cell survival, and tumor growth;MiR-130a as an oncogenic miRNA that targets PTEN to drive malignant cell survival and tumor growth</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28935812</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-130a</Data></Cell>
    <Cell><Data ss:Type="String">microRNA-130a suppresses breast cancer cell migration and invasion by targeting FOSL1 and upregulating ZO-1</Data></Cell>
    <Cell><Data ss:Type="String">MiR-130a directly targets FOSL1 and suppresses the inhibition of ZO-1, thus inhibiting cancer cell migration and invasion, in TNBCs</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29384218</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-130a</Data></Cell>
    <Cell><Data ss:Type="String">miR-130a and miR-145 reprogram Gr-1+CD11b+ myeloid cells and inhibit tumor metastasis through improved host immunity</Data></Cell>
    <Cell><Data ss:Type="String">MiR-130a targeted molecular networks including TGFβ and IGF1R pathways were correlated with higher tumor stages in cancer patients to enhance host antitumor immunity</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29973593</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-130a</Data></Cell>
    <Cell><Data ss:Type="String">The MYB/miR-130a/NDRG2 axis modulates tumor proliferation and metastatic potential in salivary adenoid cystic carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">MYB/miR-130a/NDRG2 axis, which modulates proliferation and metastasis in SACC, provides promising targets for the treatment of SACC</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30206227</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-130a</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-130a modulates a radiosensitivity of rectal cancer by targeting SOX4</Data></Cell>
    <Cell><Data ss:Type="String">MiR-130a functions as a radiosensitizer in rectal cancer and reveals a potential therapeutic target and preoperative prognostic marker for radiotherapy</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31387015</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-130a-3p</Data></Cell>
    <Cell><Data ss:Type="String">hsa-miR-130a-3p inhibits migration and invasion by regulating RAB5B in human breast cancer stem cell-like cells</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-130a-3p inhibits migration and invasion by regulating RAB5B in human breast cancer stem cell-like cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29746865</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-130a-3p</Data></Cell>
    <Cell><Data ss:Type="String">Differential expression of exosomal miRNAs between breast cancer patients with and without recurrence</Data></Cell>
    <Cell><Data ss:Type="String">Of 384 miRNAs, three miRNAs (miR-338-3p, miR-340-5p, and miR-124-3p) were significantly upregulated and eight (miR-29b-3p, miR-20b-5p, miR-17-5p, miR-130a-3p, miR-18a-5p, miR-195-5p, miR-486-5p, and miR-93-5p) were significantly downregulated in the patients with recurrence</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29050253</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-130a-3p</Data></Cell>
    <Cell><Data ss:Type="String">miR-142-5p and miR-130a-3p are regulated by IL-4 and IL-13 and control profibrogenic macrophage program</Data></Cell>
    <Cell><Data ss:Type="String">MiR-142-5p and miR-130a-3p regulate macrophage profibrogenic gene expression in chronic inflammation</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26436920</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-130a-3p</Data></Cell>
    <Cell><Data ss:Type="String">LncRNA CCAT1/miR-130a-3p axis increases cisplatin resistance in non-small-cell lung cancer cell line by targeting SOX4</Data></Cell>
    <Cell><Data ss:Type="String">CCAT1/miR-130a-3p axis enhanced DDP resistance of NSCLC cells by targeting SOX4, providing potential targets to overcome DDP resistance and improve efficacy of chemotherapy for patients with NSCLC</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29020498</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-130a-3p</Data></Cell>
    <Cell><Data ss:Type="String">MiR-130a-3p inhibits migration and invasion by regulating RAB5B in human breast cancer stem cell-like cells</Data></Cell>
    <Cell><Data ss:Type="String">MiR-130a-3p may act as a disease progression monitoring indicator and therapeutic target in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29746865</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-130a-3p</Data></Cell>
    <Cell><Data ss:Type="String">H19 Functions as a Competing Endogenous RNA to Regulate EMT by Sponging miR-130a-3p in Glioma</Data></Cell>
    <Cell><Data ss:Type="String">H19 and SOX4 are both direct target of miR-130a-3p. H19 could compete with SOX4 via sponging miR-130a-3p</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30282068</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-130a-3p</Data></Cell>
    <Cell><Data ss:Type="String">Complex role of miR-130a-3p and miR-148a-3p balance on drug resistance and tumor biology in esophageal squamous cell carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">A similar effect was observed for miR-130a-3p regulating Bcl-2 and XIAP. Our data provide the first evidence that miRNA modulation in both directions may lead to similar effects on chemotherapy response and tumor biology in esophageal squamous cell carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30510209</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-135a-3p</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-135a-3p as a promising biomarker and nucleic acid therapeutic agent for ovarian cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-135a-3p may be considered as a biomarker and a therapeutic agent in ovarian cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28231414</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-135a-3p</Data></Cell>
    <Cell><Data ss:Type="String">miR-135a inhibits tumor metastasis and angiogenesis by targeting FAK pathway</Data></Cell>
    <Cell><Data ss:Type="String">MiR-135a is a novel downstream gene of tumor suppressor p53;the expression and function of miR-135a in gastric cancer and uncovers a novel regulatory mechanism of miR-135a</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28415713</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-135a-3p</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-135a-3p is downregulated and serves as a tumour suppressor in ovarian cancer by targeting CCR2</Data></Cell>
    <Cell><Data ss:Type="String">MiR-135a-3p serves as a tumour suppressor gene in ovarian cancer by regulating CCR2</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30138893</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-135a-3p</Data></Cell>
    <Cell><Data ss:Type="String">miR-135a-3p as a promising biomarker and nucleic acid therapeutic agent for ovarian cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-135a-3p expression could be used as a noninvasive biomarker in serum of patients with ovarian carcinoma in the diagnosis and follow-up of the disease</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-145</Data></Cell>
    <Cell><Data ss:Type="String">Presence of Circulating hsa-miR-145, hsa-miR-155, and hsa-miR-382 in Exosomes Isolated from Serum of Breast Cancer Patients and Healthy Donors</Data></Cell>
    <Cell><Data ss:Type="String">Our study showed that serum-circulating miR-145, miR-155, and miR-382 are present in exosomes. These miRNAs were previously proposed as noninvasive biomarkers to distinguish between BC patients and healthy individuals</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">30891102</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-145</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-145 inhibits growth and migration of breast cancer cells through targeting oncoprotein ROCK1.</Data></Cell>
    <Cell><Data ss:Type="String">MiR-145 as a potential new diagnostic and therapeutic target for the treatment of breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26715279</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-145</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-145 inhibits growth and migration of breast cancer cells through targeting oncoprotein ROCK1.</Data></Cell>
    <Cell><Data ss:Type="String">MiR-145 acts as a tumor suppressor and its downregulation in tumor tissues may contribute to the progression of breast cancer through a mechanism involving ROCK1</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26715279</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-145</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-145 functions as a tumor suppressor by targeting matrix metalloproteinase 11 and Rab GTPase family 27a in triple-negative breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">MiR-145 might be potential therapeutic and diagnostic targets for TNBC.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27364572</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-145</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-145 functions as a tumor suppressor by targeting matrix metalloproteinase 11 and Rab GTPase family 27a in triple-negative breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">MiR-145 has an inhibitory role in TNBC malignancy by targeting MMP11 and Rab27a</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27364572</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-145</Data></Cell>
    <Cell><Data ss:Type="String">miR-145 suppresses breast cancer cell migration by targeting FSCN-1 and inhibiting epithelial-mesenchymal transition.</Data></Cell>
    <Cell><Data ss:Type="String">Ectopic expression of miR-145 significantly inhibited breast cancer cell migration.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27508031</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-145</Data></Cell>
    <Cell><Data ss:Type="String">miR-145 suppresses breast cancer cell migration by targeting FSCN-1 and inhibiting epithelial-mesenchymal transition.</Data></Cell>
    <Cell><Data ss:Type="String">MiR-145 mimic transfection enhanced the expression of FSCN-1 in Bcap-37 and HCC-1937 cells,up-regulation of miR-145 blocked EMT and decreased the expression of MMP-2/9 in breast cancer cells.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27508031</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-145</Data></Cell>
    <Cell><Data ss:Type="String">miR-145 inhibits proliferation and migration of breast cancer cells by directly or indirectly regulating TGF-β1 expression.</Data></Cell>
    <Cell><Data ss:Type="String">MiR-145 may act as a tumor-suppressor miRNA in breast cancer through inhibiting proliferation and migration of breast cancer cells. In addition, miR-145 inhibits the protein expression of TGF-β1 which may in turn contribute to tumor formation.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28393176</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-149-3p</Data></Cell>
    <Cell><Data ss:Type="String">18β-glycyrrhetinic acid suppresses gastric cancer by activation of miR-149-3p-Wnt-1 signaling</Data></Cell>
    <Cell><Data ss:Type="String">GRA inhibits the initiation and progression of gastric tumors by ameliorating the inflammatory microenvironment through downregulation of COX-2 expression and by inhibiting Wnt-1 expression through the upregulation of tumor suppressor miR-149-3p</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27713126</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-149-3p</Data></Cell>
    <Cell><Data ss:Type="String">Regulation of PLK1 through competition between hnRNPK, miR-149-3p and miR-193b-5p</Data></Cell>
    <Cell><Data ss:Type="String">HnRNPK regulates PLK1 expression by competing with the PLK1-targeting miRNAs, miR-149-3p and miR-193b-5p</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28708135</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-149-3p</Data></Cell>
    <Cell><Data ss:Type="String">Dual Strands of Pre-miR-149?Inhibit Cancer Cell Migration and Invasion through Targeting?FOXM1?in Renal Cell Carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">Dual strands of pre-miR-149 (miR-149-5p and miR-149-3p) acted as antitumor miRNAs through the targeting of FOXM1 in ccRCC cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28902136</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-149-3p</Data></Cell>
    <Cell><Data ss:Type="String">Expression of miR-149-3p inhibits proliferation, migration, and invasion of bladder cancer by targeting S100A4</Data></Cell>
    <Cell><Data ss:Type="String">S100A4 promotes cell growth, migration, and invasion and can by reversed by miR-149-3p in BCa</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29218245</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-149-3p</Data></Cell>
    <Cell><Data ss:Type="String">Characterizing the landscape of peritoneal exosomal microRNAs in patients with ovarian cancer by high-throughput sequencing</Data></Cell>
    <Cell><Data ss:Type="String">MiR-149-3p and miR-222-5p might be novel biomarkers for evaluating the prognosis of patients with EOC and that these two miRNAs might have potential therapeutic values</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30655799</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-149-3p</Data></Cell>
    <Cell><Data ss:Type="String">ZEB1-AS1 initiates a miRNA-mediated ceRNA network to facilitate gastric cancer progression</Data></Cell>
    <Cell><Data ss:Type="String">ZEB1-AS1 can interact with specific miRNAs, forming a miRNA-mediated ceRNA network and promoting GC progress, partly through a ZEB1-AS1/miR-149-3p axis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30774556</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-150-3p</Data></Cell>
    <Cell><Data ss:Type="String">Antitumor miR-150-5p and miR-150-3p inhibit cancer cell aggressiveness by targeting SPOCK1 in head and neck squamous cell carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">Downregulation of both strands of pre-miR-150 (miR-150-5p and miR-150-3p) and overexpression of SPOCK1 contribute to the aggressive nature of HNSCC. The involvement of passenger strand miRNA in the regulation of HNSCC pathogenesis is a novel concept in RNA research</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29233721</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-150-3p</Data></Cell>
    <Cell><Data ss:Type="String">MiR-150-3p targets SP1 and suppresses the growth of glioma cells</Data></Cell>
    <Cell><Data ss:Type="String">The abundance of phosphatase and tension homolog deleted on chromosome ten (PTEN), a negative downstream target of SP1, was increased with the ectopic?miR-150-3p. Collectively, these results suggested that?miR-150-3p?suppressed the growth of glioma cells partially via regulating SP1 and possibly PTEN</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29654167</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-150-3p</Data></Cell>
    <Cell><Data ss:Type="String">Molecular Pathogenesis of Gene Regulation by the miR-150 Duplex: miR-150-3p Regulates TNS4 in Lung Adenocarcinoma</Data></Cell>
    <Cell><Data ss:Type="String">Expression of TNS4 was directly regulated by miR-150-3p in LUAD cells. Aberrant expression of TNS4 was detected in LUAD clinical specimens and its aberrant expression increased the aggressiveness of LUAD cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31052206</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-155</Data></Cell>
    <Cell><Data ss:Type="String">Cancer Exosomes Perform Cell-Independent MicroRNA Biogenesis and Promote Tumorigenesis</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-155 has significantly up-regulated and has been extensively implicated in cancer progression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">25446899</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-155</Data></Cell>
    <Cell><Data ss:Type="String">Presence of Circulating hsa-miR-145, hsa-miR-155, and hsa-miR-382 in Exosomes Isolated from Serum of Breast Cancer Patients and Healthy Donors</Data></Cell>
    <Cell><Data ss:Type="String">Our study showed that serum-circulating miR-145, miR-155, and miR-382 are present in exosomes. These miRNAs were previously proposed as noninvasive biomarkers to distinguish between BC patients and healthy individuals</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">30891102</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-155</Data></Cell>
    <Cell><Data ss:Type="String">miR-155 promotes macroscopic tumor formation yet inhibits tumor dissemination from mammary fat pads to the lung by preventing EMT.</Data></Cell>
    <Cell><Data ss:Type="String">The location of tumor cells overexpressing miR-155 is a critical factor: in mammary fat pads miR-155 prevents tumor dissemination; whereas in the lung miR-155 apparently maintains the epithelial phenotype of tumor cells that is critical for macroscopic tumor formation.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21460854</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-155</Data></Cell>
    <Cell><Data ss:Type="String">miR-155 promotes macroscopic tumor formation yet inhibits tumor dissemination from mammary fat pads to the lung by preventing EMT.</Data></Cell>
    <Cell><Data ss:Type="String">Stable expression of miR-155 in 4T1 breast tumor cells reduces significantly the aggressiveness of tumor cell dissemination as a result of preventing epithelial-to-mesenchymal transition (EMT) of tumor cells in vivo. Further, miR-155 directly suppresses the expression of the transcription factor TCF4, which is an important regulator of EMT. However, when tumor cells are injected directly into the bloodstream, miR-155 remarkably promotes macroscopic tumor formation in the lung.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21460854</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-155</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-155 Regulates Cell Survival, Growth, and Chemosensitivity by Targeting FOXO3a in Breast Cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-155 is a critical therapeutic target in breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27825093</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-155</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-155 Regulates Cell Survival, Growth, and Chemosensitivity by Targeting FOXO3a in Breast Cancer</Data></Cell>
    <Cell><Data ss:Type="String">The critical role of miR-155 in regulation of cell survival and chemosensitivity through down-regulation of FOXO3a in breast cancer. Ectopic expression of miR-155 induces cell survival and chemoresistance to multiple agents, whereas knockdown of miR-155 renders cells to apoptosis and enhances chemosensitivity.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27825093</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-155</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-155, induced by FOXP3 through transcriptional repression of BRCA1, is associated with tumor initiation in human breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">A transcriptional axis of FOXP3-BRCA1-miR-155 in breast cancer cells and show that plasma miR-155 may serve as a non-invasive biomarker for detection of early stage breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28562349</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-155</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-155, induced by FOXP3 through transcriptional repression of BRCA1, is associated with tumor initiation in human breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">There was a positive correlation between expression of FOXP3 and miR-155 in breast cancer cell lines and primary breast cancers. In breast cancer cells, FOXP3 induced miR-155 through transcriptional repression of BRCA1.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28562349</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-16</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNAs are exported from malignant cells in customized particles</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-16 is characterized by excessive release from breast cancer cells while retaining relatively low concentrations of miRNA in the cells and could be used to detect the presence of malignant cells in the body</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">22772984</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-16</Data></Cell>
    <Cell><Data ss:Type="String">Exosomes derived from mesenchymal stem cells suppress angiogenesis by down-regulating VEGF expression in breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">miR-16, a miRNA known to target VEGF, was enriched in MSC-derived exosomes and it was partially responsible for the anti-angiogenic effect of MSC-derived exosomes</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">24391924</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-16</Data></Cell>
    <Cell><Data ss:Type="String">Downregulation of the tumor-suppressor miR-16 via progestin-mediated oncogenic signaling contributes to breast cancer development</Data></Cell>
    <Cell><Data ss:Type="String">MiR-16 is a tumor suppressor in progestin- and growth factor-induced growth in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22583478</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-16</Data></Cell>
    <Cell><Data ss:Type="String">Circulating microRNAs as Specific Biomarkers for Breast Cancer Detection</Data></Cell>
    <Cell><Data ss:Type="String">MiR-16, miR-21 and miR-451 in plasma of breast cancer patients has been reported as biomarker </Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23301032</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-16</Data></Cell>
    <Cell><Data ss:Type="String">MiR-16 family as potential diagnostic biomarkers for cancer: a systematic review and meta-analysis</Data></Cell>
    <Cell><Data ss:Type="String">The clinical application of miR-16 family profiling for cancers diagnosis still needs further large-scale studies and additional improvements of substantiation</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25932099</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-16</Data></Cell>
    <Cell><Data ss:Type="String">miR-16 promotes the apoptosis of human cancer cells by targeting FEAT</Data></Cell>
    <Cell><Data ss:Type="String">MiR-16 is a tumor suppressor in cancer cells through the inhibition of FEAT translation</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26031775</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-16</Data></Cell>
    <Cell><Data ss:Type="String">Global Analysis of miRNA-mRNA Interaction Network in Breast Cancer with Brain Metastasis</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-17-5p targeted mRNAs [such as BCL2, SMAD3,SOCS1 ]and pathways associated with epithelial-esenchymal transitions and other processes linked with cancer metastasis </Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28739740</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-16</Data></Cell>
    <Cell><Data ss:Type="String">MiR-16-5p targets SESN1 to regulate the p53 signaling pathway, affecting myoblast proliferation and apoptosis, and is involved in myoblast differentiation</Data></Cell>
    <Cell><Data ss:Type="String">MiR-16-5p directly targets SESN1 to regulate the p53 signaling pathway, and therefore affecting myoblast proliferation and apoptosis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29511169</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-17-5p</Data></Cell>
    <Cell><Data ss:Type="String">Differential expression of exosomal miRNAs between breast cancer patients with and without recurrence</Data></Cell>
    <Cell><Data ss:Type="String">Of 384 miRNAs, three miRNAs (miR-338-3p, miR-340-5p, and miR-124-3p) were significantly upregulated and eight (miR-29b-3p, miR-20b-5p, miR-17-5p, miR-130a-3p, miR-18a-5p, miR-195-5p, miR-486-5p, and miR-93-5p) were significantly downregulated in the patients with recurrence</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29050253</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-17-5p</Data></Cell>
    <Cell><Data ss:Type="String">Mir-17-5p Regulates Breast Cancer Cell Proliferation by Inhibiting Translation of AIB1 mRNA</Data></Cell>
    <Cell><Data ss:Type="String">Mir-17-5p, a potential translational repressor of the AIB1 oncogene, in the control of breast cancer cell proliferation</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">16940181</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-17-5p</Data></Cell>
    <Cell><Data ss:Type="String">miR-17-5p promotes human breast cancer cell migration and invasion through suppression of HBP1</Data></Cell>
    <Cell><Data ss:Type="String">MiR-17-5p plays an important role in breast cancer cell invasion and migration by suppressing HBP1 and subsequent activation of Wnt/β-catenin</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">20505989</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-17-5p</Data></Cell>
    <Cell><Data ss:Type="String">Global Analysis of miRNA-mRNA Interaction Network in Breast Cancer with Brain Metastasis</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-17-5p targeted mRNAs  such as BCL2, SMAD3,SOCS1 and pathways associated with epithelial-esenchymal transitions and other processes linked with cancer metastasis </Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28739740</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-17-5p</Data></Cell>
    <Cell><Data ss:Type="String">miR-17-5p suppresses cell proliferation and invasion by targeting ETV1 in triple-negative breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-17-5p acts as a tumour suppressor in TNBC by targeting ETV1, and a low-abundance of miR-17-5p may be involved in the pathogenesis of triple-negative breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29126392</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-17-5p</Data></Cell>
    <Cell><Data ss:Type="String">miR-106b-5p and miR-17-5p could predict recurrence and progression in breast ductal carcinoma in situ based on the transforming growth factor-beta pathway</Data></Cell>
    <Cell><Data ss:Type="String">MiR-106b-5p and miR-17-5p might have a role in breast cancer recurrence and progression by suppressing TGF-β activity, leading to early breast cancer carcinogenesis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30989460</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-181a-2-3p</Data></Cell>
    <Cell><Data ss:Type="String">let-7i-5p, miR-181a-2-3p and EGF/PI3K/SOX2 axis coordinate to maintain cancer stem cell population in cervical cancer</Data></Cell>
    <Cell><Data ss:Type="String">While the EGF pathway promotes CSC formation in cervical cancer by inducing SOX2, miR-181a-2-3p/let-7i-5p counteracts the EGF pathway by inhibiting SOX2, thereby reducing the CSC population</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29777148</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-181d-3p</Data></Cell>
    <Cell><Data ss:Type="String">Identification of common oncogenic and early developmental pathways in the ovarian carcinomas controlling by distinct prognostically significant microRNA subsets</Data></Cell>
    <Cell><Data ss:Type="String">For seven miRNAs (hsa-miR-134-3p, hsa-miR-134-5p, hsa-miR-181d-3p, hsa-miR-181d-5p, hsa-miR-494-3p, hsa-miR-494-5p, hsa-miR-517c-3p,hsa-miR-98-3p, hsa-miR-98-5p) the target mRNAs were found in micro-T-CDS only</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28984201</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-181d-3p</Data></Cell>
    <Cell><Data ss:Type="String">Upregulation of miR-125b, miR-181d, and miR-221 Predicts Poor Prognosis in MGMT Promoter-Unmethylated Glioblastoma Patients</Data></Cell>
    <Cell><Data ss:Type="String">MiR 125b-5p, miR 181d-3p, and miR 221-3p are useful in predicting poor prognosis in patients with MGMT-unmethylated glioblastomas</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29538610</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-181d-3p</Data></Cell>
    <Cell><Data ss:Type="String">MiR-376b-3p Is Associated With Long-term Response to Sunitinib in Metastatic Renal Cell Carcinoma Patients</Data></Cell>
    <Cell><Data ss:Type="String">Out of these miRNAs, miR-488-3p, miR-186-3p, miR-122-5p, miR-181d-3p, miR-615-5p and miR376b-3p were selected for further validation based on the pvalue, fold-change, average expression and available literature evidence</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31467229</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-182</Data></Cell>
    <Cell><Data ss:Type="String">hsa-miR-182,of the hsa-miR-183 cluster family,is packaged in exosomes and is detected in human exosomes from serum,breast cells and prostate cells</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-182 expression and secretion changes with breast cancer cell line aggressiveness.dependent mechanism;detectable in exosomes from human sera and may be transferred between cells via a microvesicle-dependent mechanism</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">27446418</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-182</Data></Cell>
    <Cell><Data ss:Type="String">Up-regulation of miR-182 by β-catenin in breast cancer increases tumorigenicity and invasiveness by targeting the matrix metalloproteinase inhibitor RECK</Data></Cell>
    <Cell><Data ss:Type="String">Our data demonstrate for the first time that miR-182 expression is controlled by β-catenin. In addition, we identify a new miR-182 target RECK which is important for miR-182-induced tumorigenesis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23333633</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-182</Data></Cell>
    <Cell><Data ss:Type="String">Higher expression of circulating miR-182 as a novel biomarker for breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">The current study highlights results consistent with miR-182 as a novel and valuable biomarker for the diagnosis of BC</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24260062</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-182</Data></Cell>
    <Cell><Data ss:Type="String">High expression of microRNA-183/182/96 cluster as a prognostic biomarker for breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Our findings improve our understanding of the expression level of the miR-183/182/96 cluster in breast cancer and clarify the role of the miR-183/182/96 cluster as a novel prognostic biomarker for breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27071841</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-182</Data></Cell>
    <Cell><Data ss:Type="String">MiR-182 promotes proliferation and invasion and elevates the HIF-1α-VEGF-A axis in breast cancer cells by targeting FBXW7</Data></Cell>
    <Cell><Data ss:Type="String">In conclusion, our study explores a novel mechanism by which miR-182 elevates HIF-1α expression to promote breast cancer progression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27648365</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-182</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-182 promotes proliferation and metastasis by targeting FOXF2 in triple-negative breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-182 plays an important role in the initiation and progression of TNBC by targeting FOXF2 and the miR-182/FOXF2 axis may present a new therapeutic strategy for TNBC in the future</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29085483</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-187-5p</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA deregulation in triple negative breast cancer reveals a role of miR-498 in regulating BRCA1 expression</Data></Cell>
    <Cell><Data ss:Type="String">In silico prediction revealed that miR-498 and miR-187-5p target BRCA1, and these results were confirmed by luciferase reporter assay,while miR-187-5p was found overexpressed in a luminal B cell line, miR-498 was highly expressed in a triple negative cell line, Hs578T, and its expression was negatively correlated with the levels of?BRCA1</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26933805</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-187-5p</Data></Cell>
    <Cell><Data ss:Type="String">miR-187-5p Regulates Cell Growth and Apoptosis in Acute Lymphoblastic Leukemia via DKK2</Data></Cell>
    <Cell><Data ss:Type="String">MiR-187-5p-DKK2 pathway regulates Wnt/β-catenin signaling, cell growth, and apoptosis. Our findings provide the first evidence of a role for miR-187-5p in promotion of B-cell ALL</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27296949</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-187-5p</Data></Cell>
    <Cell><Data ss:Type="String">Oncogene miR-187-5p is associated with cellular proliferation, migration, invasion, apoptosis and an increased risk of recurrence in bladder cancer</Data></Cell>
    <Cell><Data ss:Type="String">Oncogene miR-187-5p is associated with cellular proliferation, migration, invasion, apoptosis and an increased risk of recurrence in bladder cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29883941</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-187-5p</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNAs as possible indicators of drug sensitivity in breast cancer cell lines</Data></Cell>
    <Cell><Data ss:Type="String">By doing so hsa-miR-187-5p was linked to the cell cycle G2-M checkpoint in line with this checkpoint being the target of taxanes</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31063487</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-18a-5p</Data></Cell>
    <Cell><Data ss:Type="String">Differential expression of exosomal miRNAs between breast cancer patients with and without recurrence</Data></Cell>
    <Cell><Data ss:Type="String">Of 384 miRNAs, three miRNAs (miR-338-3p, miR-340-5p, and miR-124-3p) were significantly upregulated and eight (miR-29b-3p, miR-20b-5p, miR-17-5p, miR-130a-3p, miR-18a-5p, miR-195-5p, miR-486-5p, and miR-93-5p) were significantly downregulated in the patients with recurrence</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29050253</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-18a-5p</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-18a-5p functions as an oncogene by directly targeting IRF2 in lung cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-18a-5p can not only promote NSCLC by suppressing IRF2, but also will be a promising target in the near future</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28471447</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-18a-5p</Data></Cell>
    <Cell><Data ss:Type="String">SREBP1, targeted by miR-18a-5p, modulates epithelial-mesenchymal transition in breast cancer via forming a co-repressor complex with Snail and HDAC1/2</Data></Cell>
    <Cell><Data ss:Type="String">Due to crucial role of miR-18a-5p and SREBP1 in the EMT and metastasis, they provide promising drug targets for tailored therapy in the advanced breast cancer setting</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29988076</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-18a-5p</Data></Cell>
    <Cell><Data ss:Type="String">Long noncoding RNA GAS5 regulates the proliferation, migration, and invasion of glioma cells by negatively regulating miR-18a-5p</Data></Cell>
    <Cell><Data ss:Type="String">One miR-18a-5p-binding site within exon 2 of GAS5 that is partially responsible for the tumor-suppressor functions of GAS5</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30078184</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-18a-5p</Data></Cell>
    <Cell><Data ss:Type="String">Carcinogenesis of miR-18a-5p was reversed by the overexpression of IRF2 in OS</Data></Cell>
    <Cell><Data ss:Type="String">MiR-18a-5p promotes cell invasion and migration of osteosarcoma by directly targeting IRF2</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30127908</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-18a-5p</Data></Cell>
    <Cell><Data ss:Type="String">miR-18a-5p promotes cell invasion and migration of osteosarcoma by directly targeting IRF2</Data></Cell>
    <Cell><Data ss:Type="String">MiR-18a-5p promoted the invasion and migration of OS cells through inhibiting IRF2 expression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30127908</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-191</Data></Cell>
    <Cell><Data ss:Type="String">Blood Circulating Exosomes Contain Distinguishable Fractions of Free and Cell-Surface-Associated Vesicles</Data></Cell>
    <Cell><Data ss:Type="String">Preliminary data indicated that detection of cancer-specific miRNA (miR-103, miR-191, miR-195) in exosomes associated with the fraction of red blood cells allowed to discriminate HFs and BCPs more precisely compared to cell-free exosomes circulating in plasma</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">30868953</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-191</Data></Cell>
    <Cell><Data ss:Type="String">Differential expression of miR-21, miR-125b and miR-191 in breast cancer tissue.</Data></Cell>
    <Cell><Data ss:Type="String">Two miRNA (miR-125b/miR-191 and miR-21/miR-191) can discriminate between breast cancer and non-tumor tissue with high specificity and sensitivity.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22898264</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-191</Data></Cell>
    <Cell><Data ss:Type="String">Estrogen mediated-activation of miR-191/425 cluster modulates tumorigenicity of breast cancer cells depending on estrogen receptor status.</Data></Cell>
    <Cell><Data ss:Type="String">MiR-191 and miR-425 reduced proliferation, impaired tumorigenesis and metastasis, and increased expression of epithelial markers in aggressive breast cancer cells.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23505378</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-191</Data></Cell>
    <Cell><Data ss:Type="String">Estrogen mediated-activation of miR-191/425 cluster modulates tumorigenicity of breast cancer cells depending on estrogen receptor status.</Data></Cell>
    <Cell><Data ss:Type="String">MiR-191 protects ERα positive breast cancer cells from hormone starvation-induced apoptosis through the suppression of tumor-suppressor EGR1.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23505378</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-191</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-191, an estrogen-responsive microRNA, functions as an oncogenic regulator in human breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">MiR-191 as an estrogen-inducible onco-miR in breast cancer, which promotes several hallmarks of cancer including enhanced cell proliferation, migration, chemoresistance and survival in tumor microenvironment.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23542418</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-191</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-191, an estrogen-responsive microRNA, functions as an oncogenic regulator in human breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">The identification of estrogen/ER/miR-191/SATB1 cascade seems to be a significant pathway in estrogen signaling in breast cancer with miR-191 as oncogenic player.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23542418</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-191</Data></Cell>
    <Cell><Data ss:Type="String">HIF-inducible miR-191 promotes migration in breast cancer through complex regulation of TGFβ-signaling in hypoxic microenvironment.</Data></Cell>
    <Cell><Data ss:Type="String">MiR-191 enhances breast cancer aggressiveness by promoting cell proliferation, migration and survival under hypoxia.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25867965</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-191</Data></Cell>
    <Cell><Data ss:Type="String">HIF-inducible miR-191 promotes migration in breast cancer through complex regulation of TGFβ-signaling in hypoxic microenvironment.</Data></Cell>
    <Cell><Data ss:Type="String">MiR-191 is a critical regulator of transforming growth factor beta (TGFβ)-signaling and promotes cell migration by inducing TGFβ2 expression under hypoxia through direct binding and indirectly by regulating levels of a RNA binding protein, human antigen R (HuR).</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25867965</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-195</Data></Cell>
    <Cell><Data ss:Type="String">Blood Circulating Exosomes Contain Distinguishable Fractions of Free and Cell-Surface-Associated Vesicles</Data></Cell>
    <Cell><Data ss:Type="String">Preliminary data indicated that detection of cancer-specific miRNA (miR-103, miR-191, miR-195) in exosomes associated with the fraction of red blood cells allowed to discriminate HFs and BCPs more precisely compared to cell-free exosomes circulating in plasma</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">30868953</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-195</Data></Cell>
    <Cell><Data ss:Type="String">Potentially predictive microRNAs of gastric cancer with metastasis to lymph node.</Data></Cell>
    <Cell><Data ss:Type="String">MiR-212 and miR-195 could be independent biomarkers in predicting the gastric cancer with metastasis to lymph node(LN).</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21987613</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-195</Data></Cell>
    <Cell><Data ss:Type="String">Upregulation of miR-195 increases the sensitivity of breast cancer cells to Adriamycin treatment through inhibition of Raf-1</Data></Cell>
    <Cell><Data ss:Type="String">Induction of miR-195 expression promoted tumor cell apoptosis and inhibited breast cancer cell viability, but induced the sensitivity of breast cancer cells to Adriamycin treatment and was associated with inhibition of Raf-1 expression in breast cancer cells. </Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23760062</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-195</Data></Cell>
    <Cell><Data ss:Type="String">Upregulation of miR-195 increases the sensitivity of breast cancer cells to Adriamycin treatment through inhibition of Raf-1</Data></Cell>
    <Cell><Data ss:Type="String">Expression of miR-195 or knockdown of Raf-1 can similarly reduce tumor cell survival but increase apoptosis through downregulation of Raf-1 and Bcl-2 and P-glycoprotein expression. </Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23760062</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-195</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-195 inhibits proliferation, invasion and metastasis in breast cancer cells by targeting FASN, HMGCR, ACACA and CYP27B1</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-195 targets the genes of de novo lipogenesis, inhibits cell proliferation, migration, and invasion which potentially opens new avenues for the treatment of breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26632252</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-195</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-195 inhibits proliferation, invasion and metastasis in breast cancer cells by targeting FASN, HMGCR, ACACA and CYP27B1</Data></Cell>
    <Cell><Data ss:Type="String">Ectopic expression of hsa-miR-195 in MCF-7 and MDA-MB-231 cells not only altered cellular cholesterol and triglyceride levels significantly but also resulted in reduced proliferation, invasion and migration. Over expression of hsa-miR-195 decreased the Mesenchymal markers expression and enhanced Epithelial markers. </Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26632252</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-195</Data></Cell>
    <Cell><Data ss:Type="String">Expression of tumor suppressors miR-195 and let-7a as potential biomarkers of invasive breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">The analysis of miR-195 and let-7a can be used as a non-invasive biomarker for breast cancer detection.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29995098</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-195-3p</Data></Cell>
    <Cell><Data ss:Type="String">Identification of miR-195-3p as an oncogene in RCC</Data></Cell>
    <Cell><Data ss:Type="String">Knockdown of miR-195-3p induces cell apoptosis;miR-195-3p promotes cell proliferation and increases cell mobility</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28260025</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-195-3p</Data></Cell>
    <Cell><Data ss:Type="String">Prostate cancer small non-coding RNA transcriptome in Arabs</Data></Cell>
    <Cell><Data ss:Type="String">Five miRNAs are newly found to be associated with PCa namely, miR-671-3p, miR-143-5p, miR-145-3p, miR-195-3p and miR-320b. Except for miR-671-3p, all other miRNAs were found down-regulated in tumor tissues</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29268752</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-195-3p</Data></Cell>
    <Cell><Data ss:Type="String">Chemokine CCL4 induces vascular endothelial growth factor C expression and lymphangiogenesis by miR-195-3p in oral squamous cell carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">MiR-195-3p mimic reversed CCL4-enhanced VEGF-C expression. CCL4 stimulation of oral cancer cells augmented JAK2 and STAT3 phosphorylation</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29599774</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-195-5p</Data></Cell>
    <Cell><Data ss:Type="String">Differential expression of exosomal miRNAs between breast cancer patients with and without recurrence</Data></Cell>
    <Cell><Data ss:Type="String">Of 384 miRNAs, three miRNAs (miR-338-3p, miR-340-5p, and miR-124-3p) were significantly upregulated and eight (miR-29b-3p, miR-20b-5p, miR-17-5p, miR-130a-3p, miR-18a-5p, miR-195-5p, miR-486-5p, and miR-93-5p) were significantly downregulated in the patients with recurrence</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29050253</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-195-5p</Data></Cell>
    <Cell><Data ss:Type="String">Upregulation of miR-195 increases the sensitivity of breast cancer cells to Adriamycin treatment through inhibition of Raf-1</Data></Cell>
    <Cell><Data ss:Type="String">Expression of miR-195 or knockdown of Raf-1 can similarly reduce tumor cell survival but increase apoptosis through downregulation of Raf-1 and Bcl-2 and P-glycoprotein expression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23760062</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-195-5p</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-195-5p is a potential diagnostic and therapeutic target for breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Overexpression of miR-195-5p inhibited cell proliferation, reduced cell colony formation, suppressed cell migration and caused an accumulation of cells in the G1 phase of the cell cycle</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24402230</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-195-5p</Data></Cell>
    <Cell><Data ss:Type="String">Upregulation of miR-195 enhances the radiosensitivity of breast cancer cells through the inhibition of BCL-2</Data></Cell>
    <Cell><Data ss:Type="String">Exogenetic miR-195 expression could significantly enhance the radiosensitivity of human breast cancer cells; this finding may be attributed to BCL-2 downregulation to promote radiation-induced apoptosi</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26309570</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-195-5p</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-195 inhibits proliferation, invasion and metastasis in breast cancer cells by targeting FASN, HMGCR, ACACA and CYP27B1</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-195 targets the genes of de novo lipogenesis, inhibits cell proliferation, migration, and invasion which potentially opens new avenues for the treatment of breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26632252</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1972</Data></Cell>
    <Cell><Data ss:Type="String">Identification and functional characterization of the miRNA-gene regulatory network in chronic myeloid leukemia lineage negative cells</Data></Cell>
    <Cell><Data ss:Type="String">MiR-1972 induces G2-M cell cycle arrest and miR-1469 moderately arrested G1 cell cycle when overexpressed in KCL22 cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27586591</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-1972</Data></Cell>
    <Cell><Data ss:Type="String">Long noncoding RNA DANCR, working as a competitive endogenous RNA, promotes ROCK1-mediated proliferation and metastasis via decoying of miR-335-5p and miR-1972 in osteosarcoma</Data></Cell>
    <Cell><Data ss:Type="String">DNACR promoted ROCK1-meidated proliferation and metastasis through decoying both miR-335-5p and miR-1972</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29753317</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-197-5p</Data></Cell>
    <Cell><Data ss:Type="String">Comparative analysis of microRNA expression profiles between A549, A549/DDP and their respective exosomes</Data></Cell>
    <Cell><Data ss:Type="String">The expression level of 5 microRNAs (miR-197-5p, miR-4443, miR-642a-3p, miR-27b-3p and miR-100-5p) with the most differential expression were verified by qRT-PCR;microRNAs in exosomes may be involved in the drug resistance of lung cancer cells to cisplatin</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28178672</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-197-5p</Data></Cell>
    <Cell><Data ss:Type="String">miR-197-5p inhibits sarcomagenesis and induces cellular senescence via repression of KIAA0101</Data></Cell>
    <Cell><Data ss:Type="String">MiR-197-5p acts as an oncosuppressor miRNA in fibrosarcoma through target regulation of KIAA0101, which can be exploited for developing RNA-based therapeutic strategies for the cure of this malignancy</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31001891</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-200</Data></Cell>
    <Cell><Data ss:Type="String">hsa-miR-200-containing extracellular vesicles promote breast cancer cell metastasis</Data></Cell>
    <Cell><Data ss:Type="String">Promote mesenchymal-to-epithelial transition and colonisation of metastatic sites</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">28038441</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-200</Data></Cell>
    <Cell><Data ss:Type="String">miR-200 enhances mouse breast cancer cell colonization to form distant metastases</Data></Cell>
    <Cell><Data ss:Type="String">Expression of miR-200, which promotes a mesenchymal to epithelial cell transition (MET) by inhibiting Zeb2 expression, unexpectedly enhances macroscopic metastases in mouse breast cancer cell lines</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19787069</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-200</Data></Cell>
    <Cell><Data ss:Type="String">Epigenetic modulation of the miR-200 family is associated with transition to a breast cancer stem-cell-like state</Data></Cell>
    <Cell><Data ss:Type="String">These results indicate that the miR-200 family plays a crucial role in the transition between stem-like and non-stem phenotypes and that distinct epigenetic-based mechanisms regulate each miR-200 gene in this process</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23525011</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-200</Data></Cell>
    <Cell><Data ss:Type="String">MiR-200 can repress breast cancer metastasis through ZEB1-independent but moesin-dependent pathways</Data></Cell>
    <Cell><Data ss:Type="String">These findings highlight the context-dependent effects of miR-200 in breast cancer metastasis and demonstrate the existence of a moesin-dependent pathway, distinct from the ZEB1-E-cadherin axis, through which miR-200 can regulate tumour cell plasticity and metastasis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24037528</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-200</Data></Cell>
    <Cell><Data ss:Type="String">miR-200-containing extracellular vesicles promote breast cancer cell metastasis</Data></Cell>
    <Cell><Data ss:Type="String">In murine cancer and human xenograft models, miR-200-expressing tumors and extracellular vesicles from these tumors promoted metastasis of otherwise weakly metastatic cells either nearby or at distant sites and conferred to these cells the ability to colonize distant tissues in a miR-200-dependent manner</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25401471</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-200</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-200, associated with metastatic breast cancer, promotes traits of mammary luminal progenitor cells</Data></Cell>
    <Cell><Data ss:Type="String">We propose that microRNAs of the miR-200 family promote traits of highly proliferative breast luminal progenitor cells, thereby exacerbating the growth and metastatic properties of transformed mammary epithelial cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29137351</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-20b-5p</Data></Cell>
    <Cell><Data ss:Type="String">Differential expression of exosomal miRNAs between breast cancer patients with and without recurrence</Data></Cell>
    <Cell><Data ss:Type="String">Of 384 miRNAs, three miRNAs (miR-338-3p, miR-340-5p, and miR-124-3p) were significantly upregulated and eight (miR-29b-3p, miR-20b-5p, miR-17-5p, miR-130a-3p, miR-18a-5p, miR-195-5p, miR-486-5p, and miR-93-5p) were significantly downregulated in the patients with recurrence</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29050253</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-20b-5p</Data></Cell>
    <Cell><Data ss:Type="String">miR-20b modulates VEGF expression by targeting HIF-1 alpha and STAT3 in MCF-7 breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">The VEGF expression in breast cancer cells is mediated by HIF-1 and STAT3 in a miR-20b-dependent manner.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">20232316</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-20b-5p</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-20b promotes cell growth of breast cancer cells partly via targeting phosphatase and tensin homologue (PTEN)</Data></Cell>
    <Cell><Data ss:Type="String">Dysregulation of miR-20b plays critical roles in the breast cancer tumorigenesis, at least in part via targeting the tumor suppressor PTEN</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25364498</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-20b-5p</Data></Cell>
    <Cell><Data ss:Type="String">miR-20b-5p may be a biomarker for early detection and prognosis prediction, as well as a therapeutic target for RCC</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-20b-5p functions as a tumor suppressor in renal cell carcinoma by regulating cellular proliferation, migration and apoptosis</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26708577</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-20b-5p</Data></Cell>
    <Cell><Data ss:Type="String">Decreased expression of microRNA-17 and microRNA-20b promotes breast cancer resistance to taxol therapy by upregulation of NCOA3</Data></Cell>
    <Cell><Data ss:Type="String">MiR-17, miR-20b and NCOA3 may serve as some predictive biomarkers and potential therapeutic targets in taxol-resistant breast cancer treatmen</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27831559</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-21</Data></Cell>
    <Cell><Data ss:Type="String">Cancer Exosomes Perform Cell-Independent MicroRNA Biogenesis and Promote Tumorigenesis</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-21 has significantly up-regulated and has been extensively implicated in cancer progression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">25446899</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-21</Data></Cell>
    <Cell><Data ss:Type="String">Exosomal miRNA profile as complementary tool in the diagnostic and prediction of treatment response in localized breast cancer under neoadjuvant chemotherapy</Data></Cell>
    <Cell><Data ss:Type="String">Higher levels of exosomal miRNA-21, miRNA-222, and miRNA-155 were significantly associated with the presence of circulating tumor cells;Liquid biopsies based on exosomal miRNAs and circulating tumor cells can be a complementary clinical tool for improving breast cancer diagnosis and prognosis</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">30728048</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-21</Data></Cell>
    <Cell><Data ss:Type="String">Plasma exosome microRNAs are indicative of breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Based on the selective enrichment and absolute abundance, we identified miR-1246, miR-122, miR-21, and let-7a as candidate exosome microRNAs that may serve as biomarkers indicative of breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">27608715</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-21</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-21 targets tumor suppressor genes in invasion and metastasis.</Data></Cell>
    <Cell><Data ss:Type="String">Mir-21 may promote tumor invasion and metastasis by simultaneously downregulating multiple metastasis-related tumor suppressor genes operating at distinct steps of tumor progression.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">18270520</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-21</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA miR-21 overexpression in human breast cancer is associated with advanced clinical stage, lymph node metastasis and patient poor prognosis.</Data></Cell>
    <Cell><Data ss:Type="String">MiR-21 overexpression was correlated with specific breast cancer biopathologic features, such as advanced tumor stage, lymph node metastasis, and poor survival of the patients, indicating that miR-21 may serve as a molecular prognostic marker for BC and disease progression.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">18812439</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-21</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA miR-21 overexpression in human breast cancer is associated with advanced clinical stage, lymph node metastasis and patient poor prognosis.</Data></Cell>
    <Cell><Data ss:Type="String">Among the 113 BC cases, high level expression of miR-21 was significantly correlated with advanced clinical stage (P = 0.006, Fisher's exact text), lymph node metastasis (P = 0.007, Fisher's exact text), and shortened survival of the patients (hazard ratio [HR]=5.476, P &lt; 0.001).</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">18812439</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-21</Data></Cell>
    <Cell><Data ss:Type="String">High miR-21 expression in breast cancer associated with poor disease-free survival in early stage disease and high TGF-beta1.</Data></Cell>
    <Cell><Data ss:Type="String">High miR-21 was associated with poor disease-free survival in early stage patients (HR = 2.08, 95% CI: 1.08-4.00) despite no value for prognosis.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">18932017</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-21</Data></Cell>
    <Cell><Data ss:Type="String">High miR-21 expression in breast cancer associated with poor disease-free survival in early stage disease and high TGF-beta1.</Data></Cell>
    <Cell><Data ss:Type="String">Elevated miR-21 expression may facilitate tumor progression, and TGF-beta may up-regulate its expression.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">18932017</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-210</Data></Cell>
    <Cell><Data ss:Type="String">Visualization of exosome-mediated hsa-miR-210 transfer from hypoxic tumor cells</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-210 can proliferate endothelial cells and promote tumor growth and invasion</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">28038441</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-210</Data></Cell>
    <Cell><Data ss:Type="String">Hypoxic enhancement of exosome release by breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">The hypoxically regulated miR-210 was identified to be present at elevated levels in hypoxic exosome fractions</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">22998595</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-210</Data></Cell>
    <Cell><Data ss:Type="String">hsa-miR-210 overexpression is induced by hypoxia in a HIF-1alpha- and VHL-dependent fashion</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-210 Is induced by hypoxia and is an independent prognostic factor in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">18316553</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-210</Data></Cell>
    <Cell><Data ss:Type="String">hsa-miR-210 Is Induced by Hypoxia and Is an Independent Prognostic Factor in Breast Cancer</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-210 overexpression is induced by hypoxia in a HIF-1αand VHL-dependent fashion and its expression levels in breast cancer samples are an independent prognostic factor.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">18316553</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-210</Data></Cell>
    <Cell><Data ss:Type="String">hsa-miR-210 overexpression is induced by hypoxia in a HIF-1alpha- and VHL-dependent fashion</Data></Cell>
    <Cell><Data ss:Type="String">Expression levels of hsa-miR-210 in breast cancer samples are an independent prognostic factor</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">18316553</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-210</Data></Cell>
    <Cell><Data ss:Type="String">High Expression Levels of miR-21 and miR-210 Predict Unfavorable Survival in Breast Cancer: A Systemic Review and Meta-Analysis</Data></Cell>
    <Cell><Data ss:Type="String">MiRNAs such as miR-21 and miR-210 can predict poor survival rates in breast cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26349663</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-222</Data></Cell>
    <Cell><Data ss:Type="String">Exosome-mediated hsa-miR-222 transferring: An insight into NF-B-mediated breast cancer metastasis</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-222 contributes to tumorigenicity of BCa cells through down-regulation of PDLIM2 and consequently activating NF-κB</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29778754</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-222</Data></Cell>
    <Cell><Data ss:Type="String">Exosomes from Drug-Resistant Breast Cancer Cells Transmit Chemoresistance by a Horizontal Transfer of MicroRNAs</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-222-rich D/exo could alter PTEN expression in acquired cells that may spread resistance capacity </Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">24740415</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-222</Data></Cell>
    <Cell><Data ss:Type="String">Exosomal miRNA profile as complementary tool in the diagnostic and prediction of treatment response in localized breast cancer under neoadjuvant chemotherapy</Data></Cell>
    <Cell><Data ss:Type="String">Higher levels of exosomal miRNA-21, miRNA-222, and miRNA-155 were significantly associated with the presence of circulating tumor cells;Liquid biopsies based on exosomal miRNAs and circulating tumor cells can be a complementary clinical tool for improving breast cancer diagnosis and prognosis</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">30728048</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-222</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNAs miR-221 and miR-222: a new level of regulation in aggressive breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-221/222 in breast cancer metastasis, drug resistance and RAS pathways could potentially have applications in medical practice</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21888691</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-222</Data></Cell>
    <Cell><Data ss:Type="String">miR-221/222: promising biomarkers for breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-221/222 act as promising biomarkers for BCa and they would offer a new way in molecular targeting cancer treatment</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23529451</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-222</Data></Cell>
    <Cell><Data ss:Type="String">MiR-222 promotes drug-resistance of breast cancer cells to adriamycin via modulation of PTEN/Akt/FOXO1 pathway</Data></Cell>
    <Cell><Data ss:Type="String">Inhibition of miR-222 may improve the prognosis of breast cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27746366</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-222</Data></Cell>
    <Cell><Data ss:Type="String">MiR-222 promotes drug-resistance of breast cancer cells to adriamycin via modulation of PTEN/Akt/FOXO1 pathway</Data></Cell>
    <Cell><Data ss:Type="String">MiR-222 mediated ADR-resistance of breast cancer cells partly through regulation of PTEN/Akt/FOXO1 signaling pathway</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27746366</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-222</Data></Cell>
    <Cell><Data ss:Type="String">Expression Analysis of MicroRNA-222 in Breast Cancer</Data></Cell>
    <Cell><Data ss:Type="String">Our findings on miR-222 suggest that it could be a potentially useful target for control and management of breast malignancy</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29739090</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-222</Data></Cell>
    <Cell><Data ss:Type="String">miR-221/222 activate the Wnt/β-catenin signaling to promote triple-negative breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-221/222 activate the Wnt/β-catenin signaling to promote the aggressiveness and TNBC properties of breast cancers, and thus reveal a new prospect for TNBC treatment</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30053090</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-223</Data></Cell>
    <Cell><Data ss:Type="String">Microvesicles secreted by macrophages shuttle invasion-potentiating microRNAs into breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">MiR-223 promoted the invasion of breast cancer cells via the Mef2c-β-catenin pathway</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">21939504</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-223</Data></Cell>
    <Cell><Data ss:Type="String">Identification and validation of oncologic miRNA biomarkers for luminal A-like breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-29a, miR-181a, miR-223 and miR-652 were validated with altered expression in the blood of women with Luminal A-like breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24498016</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-223-3p</Data></Cell>
    <Cell><Data ss:Type="String">Exosome-encapsulated microRNA-223-3p as a minimally invasive biomarker for the early detection of invasive breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Exosomal miR-223-3p may be a useful preoperative biomarker to identify the invasive lesions of DCIS patients diagnosed by biopsy</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29805680</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-223-3p</Data></Cell>
    <Cell><Data ss:Type="String">MiR-223-3p targeting SEPT6 promotes the biological behavior of prostate cancer</Data></Cell>
    <Cell><Data ss:Type="String">Increasing SEPT6 expression might reverse the biological activity induced by miR-223-3p, which might be a potential therapeutic target for PCa</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25519054</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-223-3p</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-223-3p inhibits human bladder cancer cell migration and invasion</Data></Cell>
    <Cell><Data ss:Type="String">MiR-223-3p as a previously unrecognized microRNA that inhibits bladder carcinoma invasiveness via nuclear receptor coactivator 1, and this finding may be important for developing innovative therapeutic targets in treating bladder carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28222670</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-223-3p</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-223-3p Regulates Ovarian Cancer Cell Proliferation and Invasion by Targeting SOX11 Expression</Data></Cell>
    <Cell><Data ss:Type="String">MiR-223-3p could be a potential therapeutic for ovarian cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28587313</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-223-3p</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-223-3p Regulates Ovarian Cancer Cell Proliferation and Invasion by Targeting SOX11 Expression</Data></Cell>
    <Cell><Data ss:Type="String">MiR-223-3p regulated OC cell proliferation and invasion through targeting SOX11 expression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28587313</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-223-3p</Data></Cell>
    <Cell><Data ss:Type="String">MiR-223-3p inhibits angiogenesis and promotes resistance to cetuximab in head and neck squamous cell carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">Expression levels of miR-223-3p can be evaluated as an indicator of eligibility for non-treatment of HNSCC patients with cetuximab</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28915663</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-223-3p</Data></Cell>
    <Cell><Data ss:Type="String">MiR-223-3p functions as a tumor suppressor in lung squamous cell carcinoma by miR-223-3p-mutant p53 regulatory feedback loop</Data></Cell>
    <Cell><Data ss:Type="String">MiR-223-3p, as a tumor suppressor gene, markedly inhibited cell proliferation and migration via miR-223-3p-mutant p53 feedback loop, which suggested miR-223-3p might be a new therapeutic target in LSCC bearing p53 mutations</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30755230</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-223-3p</Data></Cell>
    <Cell><Data ss:Type="String">MiR223-3p promotes synthetic lethality in BRCA1-deficient cancers</Data></Cell>
    <Cell><Data ss:Type="String">MiR223-3p is a negative regulator of the aNHEJ DNA repair and represents a therapeutic pathway for BRCA1- or BAP1-deficient cancers</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31395736</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-25-5p</Data></Cell>
    <Cell><Data ss:Type="String">Genome-Wide Uncovering of STAT3-Mediated miRNA Expression Profiles in Colorectal Cancer Cell Lines</Data></Cell>
    <Cell><Data ss:Type="String">MiR-25-5p was the most abundant miRNA among those significantly downregulated miRNAs in both samples</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25126546</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-25-5p</Data></Cell>
    <Cell><Data ss:Type="String">Silencing protein kinase C ζ by microRNA-25-5p activates AMPK signaling and inhibits colorectal cancer cell proliferation</Data></Cell>
    <Cell><Data ss:Type="String">Exogenous expression of miR-25-5p silenced PKCζ to activate AMPK signaling, which inhibited HT-29 cell proliferation. In vivo studies showed that HT-29 xenograft growth in mice was inhibited after expressing PKCζ shRNA or miR-25-5p</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29029434</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-27a</Data></Cell>
    <Cell><Data ss:Type="String">Cancer Exosomes Perform Cell-Independent MicroRNA Biogenesis and Promote Tumorigenesis</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-27a has significantly up-regulated and has been extensively implicated in cancer progression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">25446899</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-27a</Data></Cell>
    <Cell><Data ss:Type="String">MiR-27 as a prognostic marker for breast cancer progression and patient survival.</Data></Cell>
    <Cell><Data ss:Type="String">High miR-27a expression is associated with poor overall survival in patients with breast cancer, which suggests that miR-27a could be a valuable marker of breast cancer progression.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23240057</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-27a</Data></Cell>
    <Cell><Data ss:Type="String">microRNAs miR-27a and miR-27b directly regulate liver dihydropyrimidine dehydrogenase expression through two conserved binding sites.</Data></Cell>
    <Cell><Data ss:Type="String">MiR-27a and miR-27b expression may be pharmacologically relevant modulators of DPD enzyme function in the liver.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24401318</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-27a</Data></Cell>
    <Cell><Data ss:Type="String">microRNAs miR-27a and miR-27b directly regulate liver dihydropyrimidine dehydrogenase expression through two conserved binding sites.</Data></Cell>
    <Cell><Data ss:Type="String">Increased accumulation of RNA-induced silencing complex (RISC) proteins on DPYD mRNA in cells overexpressing the highly homologous microRNAs (miRNA) miR-27a and miR-27b. These miRNAs were shown to repress DPD expression through two conserved recognition sites in DPYD.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24401318</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-27a</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-27a promotes tumorigenesis via targeting AKT in triple negative breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">MiR-27a exhibits an essential role in tumor development and progression in TNBC and may be used as a potential biomarker to predict radiotherapy response and prognosis for the disease.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29115608</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-27a</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-27a promotes tumorigenesis via targeting AKT in triple negative breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">MiR-27a inhibited radiation induced apoptosis in TNBC cells by regulation of caspase 3/7 and Bcl-2 expression. Furthermore, the expression levels of PTEN and phosphorylated protein kinase B in MDA-MB-231 and MDA?MB?468 cells was altered following overexpression of miR-27a. The luciferase assay demonstrated that miR?27a regulated PTEN and BAX expression by binding to 3'?untranslated regions.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29115608</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-27a</Data></Cell>
    <Cell><Data ss:Type="String">miR-27a promotes human breast cancer cell migration by inducing EMT in a FBXW7-dependent manner</Data></Cell>
    <Cell><Data ss:Type="String">The important function of miR-27a in regulating the metastasis of breast cancer in a FBXW7-dependent manner, and provide evidence for the potential application of miR-27a in breast cancer therapy.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30365154</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-27a</Data></Cell>
    <Cell><Data ss:Type="String">miR-27a promotes human breast cancer cell migration by inducing EMT in a FBXW7-dependent manner</Data></Cell>
    <Cell><Data ss:Type="String">Overexpression of miR-27a resulted in enhanced cell migration by inducing epithelial-to-mesenchymal transition, while its knockdown effectively reversed these cellular events.F-box and WD repeat domain containing 7 (FBXW7) is a downstream target gene of miR-27a in human breast cancer cells.the ectopic expression of FBXW7 may effectively suppress the epithelial-to-mesenchymal transition and migratory activity of breast cancer cells, in addition to reversing the cell migration mediated by miR-27a.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30365154</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-29b-3p</Data></Cell>
    <Cell><Data ss:Type="String">Differential expression of exosomal miRNAs between breast cancer patients with and without recurrence</Data></Cell>
    <Cell><Data ss:Type="String">Of 384 miRNAs, three miRNAs (miR-338-3p, miR-340-5p, and miR-124-3p) were significantly upregulated and eight (miR-29b-3p, miR-20b-5p, miR-17-5p, miR-130a-3p, miR-18a-5p, miR-195-5p, miR-486-5p, and miR-93-5p) were significantly downregulated in the patients with recurrence</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29050253</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-29b-3p</Data></Cell>
    <Cell><Data ss:Type="String">LncRNA H19/miR-29b-3p/PGRN Axis Promoted Epithelial-Mesenchymal Transition of Colorectal Cancer Cells by Acting on Wnt Signaling</Data></Cell>
    <Cell><Data ss:Type="String">The lncRNA H19/miR-29b-3p/PGRN/Wnt axis counted a great deal for seeking appropriate diagnostic biomarkers and treatment targets for CRC</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29754471</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-29b-3p</Data></Cell>
    <Cell><Data ss:Type="String">The role of lncRNA MSC-AS1/miR-29b-3p axis-mediated CDK14 modulation in pancreatic cancer proliferation and Gemcitabine-induced apoptosis</Data></Cell>
    <Cell><Data ss:Type="String">MSC-AS1/miR-29b-3p axis modulates the cell proliferation and GEM-induced cell apoptosis in PDAC cell lines through CDK14</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30915884</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-29b-3p</Data></Cell>
    <Cell><Data ss:Type="String">miR-29b-3p promotes progression of MDA-MB-231 triple-negative breast cancer cells through downregulating TRAF3</Data></Cell>
    <Cell><Data ss:Type="String">The miR-29b-3p expression was significantly increased in MDA-MB-231 compare with MCF-10A. miR-29b-3p inhibitor reduced the cell viability of MDA-MB-231 and inhibited cell migration and invasion. Cell cytoskeleton integrity destroyed after miR-29b-3p inhibitor treatment. Furthermore, we identified the mechanism and found miR-29b-3p targets the TRAF3 and activates NF-魏B signaling pathway</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31349873</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-29b-3p</Data></Cell>
    <Cell><Data ss:Type="String">Sulforaphane modulates microRNA expression in colon cancer cells to implicate the regulation of oncogenes CDC25A, HMGA2 and MYC</Data></Cell>
    <Cell><Data ss:Type="String">MiR-29b-3p is predicted to target a number of tumour-suppressing genes, further investigation of which could be informative regarding the potential of sulforaphane to suppress tumour progression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-301a</Data></Cell>
    <Cell><Data ss:Type="String">Molecular characterization of exosome-like vesicles from breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">MCF-Exo contains a higher amount of hsa-miR-301a,and overexpression has been considered a negative prognostic indicator in lymph node-negative (LNN) invasive ductal breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">24468161</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-301a</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-301 mediates proliferation and invasion in human breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-301 as a crucial oncogene in human breast cancer that acts through multiple pathways and mechanisms to promote nodal or distant relapses</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21393507</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-301a</Data></Cell>
    <Cell><Data ss:Type="String">Upregulated microRNA-301a in breast cancer promotes tumor metastasis by targeting PTEN and activating Wnt/β-catenin signaling</Data></Cell>
    <Cell><Data ss:Type="String">MiR-301a might be a potential target in breast cancer therapy</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24315818</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-301a</Data></Cell>
    <Cell><Data ss:Type="String">Upregulated microRNA-301a in breast cancer promotes tumor metastasis by targeting PTEN and activating Wnt/β-catenin signaling</Data></Cell>
    <Cell><Data ss:Type="String">MiR-301a directly targeted and suppressed PTEN, one negative regulator of the Wnt/β-catenin signaling cascade</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24315818</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-301a</Data></Cell>
    <Cell><Data ss:Type="String">Elevated miR-301a expression indicates a poor prognosis for breast cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">MiR-301a should be considered, and novel therapeutic options are needed to target this aggressive miR-301a-positive type of breast cancer to reduce recurrence and the mortality rate</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29396508</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-301a</Data></Cell>
    <Cell><Data ss:Type="String">MiR-301a-3p Suppresses Estrogen Signaling by Directly Inhibiting ESR1 in ERα Positive Breast Cancer</Data></Cell>
    <Cell><Data ss:Type="String">ESR1 as a direct target of miR-301a-3p and suggest that miR-301a-3p likely contributes to development of estrogen independence, which leads to a more invasive phenotype of breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29763890</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-301a</Data></Cell>
    <Cell><Data ss:Type="String">hsa-miR-301a- and SOX10-dependent miRNA-TF-mRNA regulatory circuits in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Regulatory motifs involving miRNAs and TFs may be useful for understanding breast cancer regulation and for predicting new biomarkers</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30814872</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-301a</Data></Cell>
    <Cell><Data ss:Type="String">hsa-miR-301a- and SOX10-dependent miRNA-TF-mRNA regulatory circuits in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">The following significant circuits were characterized and validated bioinformatically by using web-based tools: SOX10-sa-miR-301a-OXA3, SOX10-sa-miR-301a-IT, and SOX10-sa-miR-301a-FIB</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30814872</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-30a</Data></Cell>
    <Cell><Data ss:Type="String">Exosomes from Drug-Resistant Breast Cancer Cells Transmit Chemoresistance by a Horizontal Transfer of MicroRNAs</Data></Cell>
    <Cell><Data ss:Type="String">Target gene prediction and pathway analysis showed the involvement of miR-100, miR-222, and miR-30a in pathways implicated in cancer pathogenesis, membrane vesiculation and therapy failure,the transmition of chemoresistance by a horizontal transfer of miRNAs</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">24740415</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-30a</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA miR-30 family regulates non-attachment growth of breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">MiR30-family regulates the growth of breast cancer cells in non-attachment conditions</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23445407</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-30a</Data></Cell>
    <Cell><Data ss:Type="String">miR-30a suppresses breast cancer cell proliferation and migration by targeting Eya2</Data></Cell>
    <Cell><Data ss:Type="String">MiR-30a/Eya2 axis may play an important role in breast cancer development and progression and that miR-30a activation or Eya2 inhibition may be a useful strategy for cancer treatment</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24508260</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-30a</Data></Cell>
    <Cell><Data ss:Type="String">The Versatile Role of microRNA-30a in Human Cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-30a may serve as a potential target in the diagnosis and therapy of human cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28359057</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-30a</Data></Cell>
    <Cell><Data ss:Type="String">miR-30a inhibits the biological function of breast cancer cells by targeting Notch1</Data></Cell>
    <Cell><Data ss:Type="String">MiR-30a attenuates the development of breast cancer by regulating the expression of the downstream target gene, Notch1</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28765900</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-30a</Data></Cell>
    <Cell><Data ss:Type="String">A p53/miR-30a/ZEB2 axis controls triple negative breast cancer aggressiveness</Data></Cell>
    <Cell><Data ss:Type="String">The existence of a novel axis linking p53 to EMT via miR-30a, and adds support to the notion that miRNAs represent key elements of the complex network whereby p53 inactivation affects TNBC clinical behavior</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29666469</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-31</Data></Cell>
    <Cell><Data ss:Type="String">hsa-miR-31 shuttled by halofuginone-induced exosomes suppresses MFC-7 cell proliferation by modulating the HDAC2/cell cycle signaling axis</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-31 modulates MCF-7 cells growth by specially targeting the histone deacetylase 2</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">30916359</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-31</Data></Cell>
    <Cell><Data ss:Type="String">A Pleiotropically Acting microRNA, miR-31, Inhibits Breast Cancer Metastasis</Data></Cell>
    <Cell><Data ss:Type="String">MiR-31 uses multiple mechanisms to oppose metastasis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19524507</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-31</Data></Cell>
    <Cell><Data ss:Type="String">miR-155 and miR-31 are differentially expressed in breast cancer patients and are correlated with the estrogen receptor and progesterone receptor status</Data></Cell>
    <Cell><Data ss:Type="String">These results suggest that miR-155 and miR-31 are differentially expressed in breast cancer patients. Their correlation with the clinicopathological characteristics may aid the diagnosis and treatment of invasive intraductal breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23162645</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-31</Data></Cell>
    <Cell><Data ss:Type="String">A novel mechanism of regulation of the anti-metastatic miR-31 by EMSY in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">This regulation is dependent on the DNA-binding transcription factor ETS-1 which recruits EMSY and the histone demethylase KDM5B to the miR-31 promoter, thus repressing its transcription</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25927669</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-31</Data></Cell>
    <Cell><Data ss:Type="String">MiR-31 inhibits migration and invasion by targeting SATB2 in triple negative breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-31 inhibited TNBC cells migration and invasion through suppressing SATB2 expression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27593563</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3126-3p</Data></Cell>
    <Cell><Data ss:Type="String">Evaluation of Plasma Extracellular Vesicle MicroRNA Signatures for Lung Adenocarcinoma and Granuloma With Monte-Carlo Feature Selection Method</Data></Cell>
    <Cell><Data ss:Type="String">In EV, the top 10 discriminative miRNAs were hsa-miR-23b-3p, hsa-miR-548ac, hsa-miR-3126-3p, hsa-miR-15b-5p, hsa-miR-205-5p, hsa-miR-5010-5p, hsa-miR-331-5p, hsa-miR-1249-3p, hsa-miR-548c-5p, and hsa-miR-1827</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31105742</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3147</Data></Cell>
    <Cell><Data ss:Type="String">Serum microRNA expression levels can predict lymph node metastasis in patients with early-stage cervical squamous cell carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">Serum miR-3147 expression levels can predict metastasis in patients with early-stage cervical squamous cell carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23799609</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3147</Data></Cell>
    <Cell><Data ss:Type="String">miR-3147 serves as an oncomiR in vulvar squamous cell cancer via Smad4 suppression</Data></Cell>
    <Cell><Data ss:Type="String">MiR-3147 may represent a novel potential therapeutic target marker for VSCC.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29512734</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3147</Data></Cell>
    <Cell><Data ss:Type="String">miR-3147 serves as an oncomiR in vulvar squamous cell cancer via Smad4 suppression</Data></Cell>
    <Cell><Data ss:Type="String">MiR-3147 may serve an oncogenic role in VSCC by targeting Smad4</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29512734</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3151-5p</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNAs Responsible for Inflammation in Obesity</Data></Cell>
    <Cell><Data ss:Type="String">The analysis identified 19 high scoring microRNAs (miR-146, miR-378, miR-143, miR-145, miR-194, miR-1273, miR-190, miR-561, miR-151, miR-215, miR-196, miR-328, miR-208, miR-3155A, miR-933, miR-4685, miR-640, miR-4659, and miR-877)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3153</Data></Cell>
    <Cell><Data ss:Type="String">Antroquinonol inhibits NSCLC proliferation by altering PI3K/mTOR proteins and miRNA expression profiles</Data></Cell>
    <Cell><Data ss:Type="String">Twelve miRNAs were downregulated (miR-10a, miR-135a, miR-299-3p, miR-3126-5p, miR-3153, miR-411, miR-4321, miR-486-5p, miR-505, miR-598, miR-601, miR-939) after antroquinonol treatment</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21185843</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3153</Data></Cell>
    <Cell><Data ss:Type="String">Plasma microRNA alterations between EGFR-activating mutational NSCLC patients with and without primary resistance to TKI</Data></Cell>
    <Cell><Data ss:Type="String">MiRNA microarray of plasma from patients' blood identified 16 differentially expressed miRNAs of which 15 (hsv2-miR-H19, hsa-miR-744-5p, hsa-miR-3196, hsa-miR-3153, hsa-miR-4791, hsa-miR-4803, hsa-miR-4796-3p, hsa-miR-372-5p, hsa-miR-138-2-3p, hsa-miR-16-1-3p, hsa-miR-1469, hsa-miR-585-3p, ebv-miR-BART14-5p, hsa-miR-769-3p, hsa-miR-548aq-5p) were down regulated while only hsa-miR-503-3p was up regulated in primary resistant patients' plasma</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29179454</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3155a</Data></Cell>
    <Cell><Data ss:Type="String">MiRNA-3670 and miR-8078 Induce the Apoptosis Mediated by SERPINB5 in Lung Cancers</Data></Cell>
    <Cell><Data ss:Type="String">MiRNA-3670 and miR-8078 Induce the Apoptosis Mediated by SERPINB5 in Lung Cancers</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3161</Data></Cell>
    <Cell><Data ss:Type="String">Differential exosomal microRNA profile in the serum of a patient with depression NCBI</Data></Cell>
    <Cell><Data ss:Type="String">There were 12 up-regulated miRNAs: hsa-miR-1255a, hsa-miR-3161, hsa-miR-99a-3p, hsa-miR-205-5p, hsa-miR-26a-1-3p, hsa-miR-139-5p, hsa-miR-7849-3p, hsa-miR-195-5p, hsa-miR-125b-2-3p, hsa-miR-664a-3p, hsa-let-7c-5p, and hsa-miR-197-3p.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29050253</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3161</Data></Cell>
    <Cell><Data ss:Type="String">Overexpression of miRNA 4451 is Associated With a Poor Survival of Patients With Hypopharyngeal Cancer After Surgery With Postoperative Radiotherapy</Data></Cell>
    <Cell><Data ss:Type="String">MiR-200c, miR-429, and miR-4701 were down-regulated, whereas miR-3161, miR-3605-5p, miR-378b, and miR-4451 were up-regulated in the death group compared with those in the alive group</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30103154</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3161</Data></Cell>
    <Cell><Data ss:Type="String">Identification of miR-708-5p in peripheral blood monocytes: Potential marker for postmenopausal osteoporosis in Mexican-Mestizo population</Data></Cell>
    <Cell><Data ss:Type="String">We identified six candidate microRNAs: four were up-regulated (miR-708-5p, miR-34b-5p, miR-3161, miR-328-5p), while two were down-regulated (miR-4422 and miR-939-3p) in osteoporotic women</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30322266</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3175</Data></Cell>
    <Cell><Data ss:Type="String">Primary analysis and screening of microRNAs in gastric cancer side population cells</Data></Cell>
    <Cell><Data ss:Type="String">There are key miRNAs expressed within the SP cells of the gastric cancer cell line MKN-45, and include hsa-miR-3175, hsa-miR-203, hsa-miR-130a, hsa-miR-324-5p, hsa-miR-34a, and hsa-miR-25-star</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25834316</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3175</Data></Cell>
    <Cell><Data ss:Type="String">Detection of Potential Metastatic Prostate Cancer Circulating Biomarkers by Comparison of miRNA Profiles in DU145 Cells and Culture Medium</Data></Cell>
    <Cell><Data ss:Type="String">Three of these miRNA, hsa-miR-4417, hsa-miR-3175, and hsa-miR-6782-5p, exhibit the highest expression and are candidate circulating biomarkers for metastatic activity of prostate cancer.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28429232</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3176</Data></Cell>
    <Cell><Data ss:Type="String">Exosome-derived microRNAs contribute to prostate cancer chemoresistance</Data></Cell>
    <Cell><Data ss:Type="String">The hub AR and PTEN target genes mainly regulated by upregulated miRNAs (hsa-miR-16-5p, -23c, -32-5p, -3915, -5004-5p, -488-3p, -3673 and -3654) and downregulated miRNAs (hsa-miR-3176 and -141-3p)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27278879</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3176</Data></Cell>
    <Cell><Data ss:Type="String">A microRNA expression signature for clinical response in locally advanced cervical cancer</Data></Cell>
    <Cell><Data ss:Type="String">The miRNAs reported here, including miR-3176, miR-3676, miR-502, miR-128, miR-145, miR-651, miR-299, miR-548, and miR-345, are for the first time associated with the development of resistance in LACC patients</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27423381</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3185</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA expressions associated with progression of prostate cancer cells to antiandrogen therapy resistance</Data></Cell>
    <Cell><Data ss:Type="String">MiRNAs -454, -3131 and -3185 are noted for the first time to be deregulated during progression of CRPC</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24387052</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3185</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNAs are part of the regulatory network that controls EGF induced apoptosis, including elements of the JAK/STAT pathway, in A431 cells</Data></Cell>
    <Cell><Data ss:Type="String">MiRNAs (miR-663, miR-499-5p, miR-494, miR-602, miR-2861, miR-675 and miR-3185) may have crucial functions in A431 cell apoptosis through a process involving epidermal growth factor (EGF) involvement</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25781916</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3185</Data></Cell>
    <Cell><Data ss:Type="String">microRNA miR-3185 mediated alternative translation initiation of peroxiredoxin 5 mRNA in human breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">Increase in the oxidation state leads to an increased expression of hsa-miR-3185. Increase amount of miR-3185 leads to an increase in short form of PRDX5 translation from the second AUG perhaps by blocking the translation initiation from the first AUG codon</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3188</Data></Cell>
    <Cell><Data ss:Type="String">miR-3188 regulates nasopharyngeal carcinoma proliferation and chemosensitivity through a FOXO1-modulated positive feedback loop with mTOR-PI3K/AKT-c-JUN</Data></Cell>
    <Cell><Data ss:Type="String">As a tumour suppressor, miR-3188 directly targets mTOR to stimulate its own expression and participates in FOXO1-mediated repression of cell growth, tumorigenesis and NPC chemotherapy resistance</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27095304</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3188</Data></Cell>
    <Cell><Data ss:Type="String">miR-3188 Regulates Cell Proliferation, Apoptosis, and Migration in Breast Cancer by Targeting TUSC5 and Regulating the p38 MAPK Signaling Pathway</Data></Cell>
    <Cell><Data ss:Type="String">MiR-3188 may serve as a potential therapeutic agent for the treatment of breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28560951</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3188</Data></Cell>
    <Cell><Data ss:Type="String">miR-3188 Regulates Cell Proliferation, Apoptosis, and Migration in Breast Cancer by Targeting TUSC5 and Regulating the p38 MAPK Signaling Pathway</Data></Cell>
    <Cell><Data ss:Type="String">MiR-3188 affects breast cancer cell proliferation, apoptosis, and migration by targeting TUSC5 and activating the p38 MAPK signaling pathway</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28560951</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3188</Data></Cell>
    <Cell><Data ss:Type="String">Hepatitis B virus X protein promotes CREB-mediated activation of miR-3188 and Notch signaling in hepatocellular carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">The HBx-miR-3188-ZHX2-Notch1 signaling pathway plays an important role in the pathogenesis and progression of HBV-related HCC with family history of HCC</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28574502</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3188</Data></Cell>
    <Cell><Data ss:Type="String">MiR-3188 Inhibits Non-small Cell Lung Cancer Cell Proliferation Through FOXO1-Mediated mTOR-p-PI3K/AKT-c-JUN Signaling Pathway</Data></Cell>
    <Cell><Data ss:Type="String">MiR-3188 interacts with mTOR and FOXO1 to inhibit NSCLC cell proliferation through a mTOR-p-PI3K/AKT-c-JUN signaling pathway</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30618730</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3188</Data></Cell>
    <Cell><Data ss:Type="String">Loss of exosomal miR-3188 in cancer-associated fibroblasts contributes to HNC progression</Data></Cell>
    <Cell><Data ss:Type="String">The potential therapeutic value of exosomal miR-3188 for inhibiting HNC growth.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30961650</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3196</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-3196 is inhibited by H2AX phosphorylation and attenuates lung cancer cell apoptosis by downregulating PUM</Data></Cell>
    <Cell><Data ss:Type="String">H2AX phosphorylation regulates apoptosis in lung cancer cells via the miR-3196/PUMA pathway</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27780918</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3196</Data></Cell>
    <Cell><Data ss:Type="String">Overexpression of miR-3196 suppresses cell proliferation and induces cell apoptosis through targeting ERBB3 in breast?cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-3196 can serve as a potential biomarker and therapeutic target for breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30556879</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3196</Data></Cell>
    <Cell><Data ss:Type="String">Overexpression of miR-3196 suppresses cell proliferation and induces cell apoptosis through targeting ERBB3 in breast?cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-3196 was lowly expressed in breast cancer tissues. Overexpression of miR-3196 could repress the proliferation and induce the apoptosis of breast cancer cells via targeting the 3'UTR of ERBB3</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30556879</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3196</Data></Cell>
    <Cell><Data ss:Type="String">Long noncoding RNA ADPGK-AS1 promotes cell proliferation, migration, and EMT process through regulating miR-3196/OTX1 axis in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">ADPGK-AS1 acted as a competing endogenous RNA (ceRNA) via modulating miR-3196/OTX1 axis in BC</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31264061</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3196</Data></Cell>
    <Cell><Data ss:Type="String">Genome-wide analysis of microRNA signature in lung adenocarcinoma with EGFR exon 19 deletion</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNAs associate with EGFR exon 19 deletion and miR-3196 can be further explored for potential predictor and targeted biomarker when it is difficult to get the tumors</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-328</Data></Cell>
    <Cell><Data ss:Type="String">Molecular characterization of exosome-like vesicles from breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">MDA-Exo also contains significant amounts of hsa-miR-328,which has been shown to target CD44,reduce cell adhesion,enhance cell migration and regulate capillary structure formation</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">24468161</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-328</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-328 negatively regulates the expression of breast cancer resistance protein (BCRP/ABCG2) in human cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">MiR-328 targets ABCG2 3'-UTR and controls ABCG2 protein expression and influences drug disposition in human breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19270061</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-328</Data></Cell>
    <Cell><Data ss:Type="String">Breast cancer resistance protein BCRP/ABCG2 regulatory microRNAs (hsa-miR-328, -519c and -520h) and their differential expression in stem-like ABCG2+ cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">MiR-519c and -328 have greater impact on ABCG2 expression than miR-520h in MCF-7 human breast cancer cells, and the presence of proximal miR-519c MRE explains the action of miR-519c on shortened ABCG2 3'UTR</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21219875</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-328</Data></Cell>
    <Cell><Data ss:Type="String">Prognostic microRNA/mRNA signature from the integrated analysis of patients with invasive breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">The prognostic RNAs included PIK3CA, one of the two most frequently mutated genes in IDC, and miRNAs such as hsa-miR-328, hsa-miR-484, and hsa-miR-874</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23589849</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-338-3p</Data></Cell>
    <Cell><Data ss:Type="String">Differential expression of exosomal miRNAs between breast cancer patients with and without recurrence</Data></Cell>
    <Cell><Data ss:Type="String">Of 384 miRNAs, three miRNAs (miR-338-3p, miR-340-5p, and miR-124-3p) were significantly upregulated and eight (miR-29b-3p, miR-20b-5p, miR-17-5p, miR-130a-3p, miR-18a-5p, miR-195-5p, miR-486-5p, and miR-93-5p) were significantly downregulated in the patients with recurrence</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29050253</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-338-3p</Data></Cell>
    <Cell><Data ss:Type="String">miR-338-3p Suppresses Gastric Cancer Progression through a PTEN-AKT Axis by Targeting P-REX2a</Data></Cell>
    <Cell><Data ss:Type="String">MiR-338-3p affects gastric cancer progression through PTEN-AKT signaling by targeting P-Rex2a in gastric cancer cells, which posits miR-338-3p as a novel strategy for gastric cancer treatment</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24375644</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-338-3p</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-338-3p functions as tumor suppressor in breast cancer by targeting SOX4</Data></Cell>
    <Cell><Data ss:Type="String">MiR-338-3p may act as a tumor suppressor in breast cancer by targeting SOX4, suggesting miR?338-3p as a novel strategy for breast cancer treatment</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26252944</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-338-3p</Data></Cell>
    <Cell><Data ss:Type="String">The EGFR/miR-338-3p/EYA2 axis controls breast tumor growth and lung metastasis</Data></Cell>
    <Cell><Data ss:Type="String">MiR-338-3p/EYA2 axis contributes to EGFR-mediated tumor growth and lung metastasis and that miR-338-3p activation or EYA2 inhibition or combination therapy targeting EGFR/miR-338-3p/EYA2 axis may be a promising way to treat patients with metastatic cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28703807</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-338-3p</Data></Cell>
    <Cell><Data ss:Type="String">miR-338-3p inhibits the invasion of renal cell carcinoma by downregulation of ALK5</Data></Cell>
    <Cell><Data ss:Type="String">MiR-338-3p acts as a novel tumor suppressor to inhibit the invasion of RCC by regulating ALK5 expression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28969055</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-338-3p</Data></Cell>
    <Cell><Data ss:Type="String">miR-338-3p targets RAB23 and suppresses tumorigenicity of prostate cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">MiR-338-3p acts as a tumor suppressor in prostate cancer by directly targetingRAB23</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30662812</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-340-5p</Data></Cell>
    <Cell><Data ss:Type="String">Differential expression of exosomal miRNAs between breast cancer patients with and without recurrence</Data></Cell>
    <Cell><Data ss:Type="String">Of 384 miRNAs, three miRNAs (miR-338-3p, miR-340-5p, and miR-124-3p) were significantly upregulated and eight (miR-29b-3p, miR-20b-5p, miR-17-5p, miR-130a-3p, miR-18a-5p, miR-195-5p, miR-486-5p, and miR-93-5p) were significantly downregulated in the patients with recurrence</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29050253</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-340-5p</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-340-5p modulates cisplatin resistance by targeting LPAATβ in osteosarcoma</Data></Cell>
    <Cell><Data ss:Type="String">MiR-340-5p enhanced the sensitivity to CDDP by targeting LPAATβ</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28443990</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-340-5p</Data></Cell>
    <Cell><Data ss:Type="String">MiR-340-5p is a potential prognostic indicator of colorectal cancer and modulates ANXA3</Data></Cell>
    <Cell><Data ss:Type="String">MiR-340-5p might represent a novel prognostic biomarker and therapeutic target for CRC</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30070320</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-340-5p</Data></Cell>
    <Cell><Data ss:Type="String">MiR-340-5p is a potential prognostic indicator of colorectal cancer and modulates ANXA3</Data></Cell>
    <Cell><Data ss:Type="String">MiR-340-5p exerted its tumor-suppressive function by directly targeting ANXA3 in CRC</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30070320</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-340-5p</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-340-5p suppresses non-small cell lung cancer cell growth and metastasis by targeting ZNF503</Data></Cell>
    <Cell><Data ss:Type="String">MiR-340-5p inhibits NCI-H1650 cell proliferation and invasion by directly targeting ZNF503 and that miR-340-5p can serve as a potential therapeutic target for treating NSCLC</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31160893</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-340-5p</Data></Cell>
    <Cell><Data ss:Type="String">miR-340-5p Suppresses Aggressiveness in Glioblastoma Multiforme by Targeting Bcl-w and Sox2</Data></Cell>
    <Cell><Data ss:Type="String">Our novel findings highlight the potential utility of miR-340-5p as a therapeutic agent for glioblastoma multiforme through inhibitory effects on Bcl-w-induced PDGF-A and Sox2 activation</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31272074</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-34a</Data></Cell>
    <Cell><Data ss:Type="String">Molecular characterization of exosome-like vesicles from breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">MCF-Exo also contains mir-34a, which regulates several genes including p53</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">24468161</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-34a</Data></Cell>
    <Cell><Data ss:Type="String">MiR-34a expression has an effect for lower risk of metastasis and associates with expression patterns predicting clinical outcome in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-34a expression activation is a marker of aggressive breast tumour phenotype it exerts an independent effect for a lower risk of recurrence or death from breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22102859</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-34a</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-34a: a potential therapeutic target in human cancer</Data></Cell>
    <Cell><Data ss:Type="String">Early studies have shown that miR-34a acts as a tumor-suppressor gene by targeting many oncogenes related to proliferation, apoptosis and invasion</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25032850</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-34a</Data></Cell>
    <Cell><Data ss:Type="String">The diagnostic role of microRNA-34a in breast cancer: a systematic review and meta-analysis</Data></Cell>
    <Cell><Data ss:Type="String">MiR-34a is a promising non-invasive biomarker in diagnosing BC</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28423566</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-34a</Data></Cell>
    <Cell><Data ss:Type="String">miR-34a directly targets tRNAiMet?precursors and affects cellular proliferation, cell cycle, and apoptosis</Data></Cell>
    <Cell><Data ss:Type="String">MiR-34a directly targets tRNAiMet precursors via AGO2-mediated cleavage, and that tRNAiMet functions as an oncogene, potentially representing a target molecule for therapeutic intervention</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29941603</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-34a</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-34 family in breast cancer: from research to therapeutic potential</Data></Cell>
    <Cell><Data ss:Type="String">MiR-34s will open new opportunities for the development of novel therapeutic strategies and define a new approach in identifying potential biomarkers for early diagnosis of breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30405848</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-34a</Data></Cell>
    <Cell><Data ss:Type="String">Evaluation of miRNA-9 and miRNA-34a as potential biomarkers for diagnosis of breast cancer in Iranian women</Data></Cell>
    <Cell><Data ss:Type="String">MiR-9 and miR-34a have the capability for distinguishing tumor tissues from healthy tissues and the study of their expression levels in tissue may be used as a biomarker for the diagnosis of breast cancer patients from healthy women</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30468908</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-34a</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA 34a suppresses breast cancer cell proliferation and invasion by targeting Notch1</Data></Cell>
    <Cell><Data ss:Type="String">MiR-34a inhibitor transfection resulted in the opposite effects. In conclusion, the presented data indicated that miR-34a suppressed breast cancer cell proliferation and invasion, and its effect may partly be exerted by targeting Notch1</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30542388</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-34a</Data></Cell>
    <Cell><Data ss:Type="String">Overexpression of miR-34a and miR-16 Synergistically Promotes Apoptosis in Breast Cancer Cells</Data></Cell>
    <Cell><Data ss:Type="String">MiR-16 or miR-34a induced apoptosis individually</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3622a-5p</Data></Cell>
    <Cell><Data ss:Type="String">A novel microRNA regulator of prostate cancer epithelial-esenchymal transition</Data></Cell>
    <Cell><Data ss:Type="String">Here we provide the first direct evidence that miR-3622a-5p (major form of miR-3622a, referred to as miR-3622a) inhibits PCa EMT, progression and metastasis;we found that miR-3622a directly targets EMT effectors ZEB1 and SNAI2;miR-3622a is a novel PCa biomarker and potential drug target for developing therapeutic regimens against advanced PCa</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28498363</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3622a-5p</Data></Cell>
    <Cell><Data ss:Type="String">Aberrantly Expressed Genes and miRNAs in Slow Transit Constipation Based on RNA-Seq Analysis</Data></Cell>
    <Cell><Data ss:Type="String">Downregulated expression of hsa-miR-3622a-5p in colon tissue of STC. And adrenoceptor alpha (ADRA1D) was one of target genes of hsa-miR-3622a-5p in STC</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30186855</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3654</Data></Cell>
    <Cell><Data ss:Type="String">Exosome-derived microRNAs contribute to prostate cancer chemoresistance</Data></Cell>
    <Cell><Data ss:Type="String">We found that hub hsa-16-5p, hsa-miR-3915, hsa-miR-488-3p, hsa-miR-5004-5p, hsa-miR-23c, hsa-miR-3673, hsa-miR-3654, and hsa-miR-32-5p were potential targets to hub androgen receptor (AR) and phosphatase and tensin homolog (PTEN)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27278879</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3654</Data></Cell>
    <Cell><Data ss:Type="String">In Silico Identification of Human miR 3654 and its Targets Revealed its Involvement in Prostate Cancer Progression</Data></Cell>
    <Cell><Data ss:Type="String">MiR-3654 involved in prostate cancer progression using computational approach and hypothesized that the down regulation of miR-3654 could be responsible for a solid tumor to get cancer stem-like cell phenotype</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27297584</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3663-3p</Data></Cell>
    <Cell><Data ss:Type="String">Comparative microarray analysis of microRNA expression profiles in primary cutaneous malignant melanoma, cutaneous malignant melanoma metastases, and benign melanocytic nevi</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-3663-3p and -4281 conversely were found upregulated in malignant melanoma</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23111773</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3663-3p</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA expression profiling in placenta and maternal plasma in early pregnancy loss</Data></Cell>
    <Cell><Data ss:Type="String">The comparison between EPL and control group samples by microarray and RT-qPCR revealed that miR-125a-3p, miR-3663-3p and miR-575 were significantly upregulated in tissue samples</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29393376</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3667-5p</Data></Cell>
    <Cell><Data ss:Type="String">Association of Cigarette Smoking and microRNA Expression in Rectal Cancer: Insight into Tumor Phenotype</Data></Cell>
    <Cell><Data ss:Type="String">Eight of the miRNAs (hsa-miR-139-3p, hsa-miR-3667-5p, hsa-miR-425-3p, hsa-miR-4298, hsa-miR-4429, hsa-miR-4481, hsa-miR-4685-5p, and hsa-miR-4783-3p) increased risk of colorectal cancer death among rectal cancer cases with expression increases in carcinoma tissue, and these miRNAs had higher expression in carcinoma tissue with subjects who smoked more pack-years</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27780077</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3690</Data></Cell>
    <Cell><Data ss:Type="String">Alcohol-dysregulated miR-30a and miR-934 in head and neck squamous cell carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">MiR-3164 and miR-3690 demonstrate no previous connections to cancer, establishing them as potentially fruitful targets for future investigation</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26472042</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3690</Data></Cell>
    <Cell><Data ss:Type="String">Integrated genomic analysis for prediction of survival for patients with liver cancer using The Cancer Genome Atlas</Data></Cell>
    <Cell><Data ss:Type="String">MiR-3690, miR-561 and miR-621 were independent prognostic factors for the liver cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30065560</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-372</Data></Cell>
    <Cell><Data ss:Type="String">Increased serum levels of circulating exosomal microRNA-373 in receptor-negative breast cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">The levels of exosomal miR-101 and miR-372 were tumor-specifically increased and higher in breast cancer patients than in healthy women</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">25333260</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-372</Data></Cell>
    <Cell><Data ss:Type="String">Multiple targets of miR-302 and miR-372 promote reprogramming of human fibroblasts to induced pluripotent stem cells</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-302b and hsa-miR-372 promote human somatic cell reprogramming</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21490602</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-372</Data></Cell>
    <Cell><Data ss:Type="String">miR-372 down-regulates the oncogene ATAD2 to influence hepatocellular carcinoma proliferation and metastasis</Data></Cell>
    <Cell><Data ss:Type="String">MiR-372 suppressed the expression of ATAD2, which was highly expressed in HCC and exerted a proto-oncogene effect in hepatic carcinogenesis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24552534</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-372</Data></Cell>
    <Cell><Data ss:Type="String">Low mir-372 expression correlates with poor prognosis and tumor metastasis in hepatocellular carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">MiR-372 may play an important role in hepatic carcinogenesis and may serve as a new target or method to detect and treat HCC in the future</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25880458</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-372</Data></Cell>
    <Cell><Data ss:Type="String">miR-372 suppresses tumour proliferation and invasion by targeting IGF2BP1 in renal cell carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">MiR-372 seemed to function as a tumour suppressor in renal cell carcinoma progression by inhibiting the IGF2BP1 expression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26332146</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-372</Data></Cell>
    <Cell><Data ss:Type="String">miR-372 promotes breast cancer cell proliferation by directly targeting LATS2</Data></Cell>
    <Cell><Data ss:Type="String">MiR-372 functions as an oncogenic miRNA in breast cancer by targeting LATS2</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29456685</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-372</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA expression profile in HER2-positive breast cancer patients submitted to neoadjuvant chemotherapy.</Data></Cell>
    <Cell><Data ss:Type="String">Mir-135b, mir-372 and mir-520h as potential candidates markers for trastuzumab resistance in HER2-positive breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-373</Data></Cell>
    <Cell><Data ss:Type="String">Cancer Exosomes Perform Cell-Independent MicroRNA Biogenesis and Promote Tumorigenesis</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-373 has significantly up-regulated and has been extensively implicated in cancer progression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">25446899</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-373</Data></Cell>
    <Cell><Data ss:Type="String">Increased serum levels of circulating exosomal microRNA-373 in receptor-negative breast cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">In conclusion, our findings suggest cell-free miR-101 and miR-373 as breast cancer-specific markers</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">25333260</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-373</Data></Cell>
    <Cell><Data ss:Type="String">The microRNAs miR-373 and miR-520c promote tumour invasion and metastasis.</Data></Cell>
    <Cell><Data ss:Type="String">MiR-373 and miR-520c stimulated cancer cell migration and invasion in vitro and in vivo, and that certain cancer cell lines depend on endogenous miR-373 activity to migrate efficiently.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">18193036</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-373</Data></Cell>
    <Cell><Data ss:Type="String">The microRNAs miR-373 and miR-520c promote tumour invasion and metastasis.</Data></Cell>
    <Cell><Data ss:Type="String">The migration phenotype of miR-373 and miR-520c can be explained by suppression of CD44,significant upregulation of miR-373 in clinical breast cancer metastasis samples that correlated inversely with CD44 expression.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">18193036</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-373</Data></Cell>
    <Cell><Data ss:Type="String">The level of circulating miRNA-10b and miRNA-373 in detecting lymph node metastasis of breast cancer: potential biomarkers.</Data></Cell>
    <Cell><Data ss:Type="String">Circulating miRNA-10b and miRNA-373 are potential biomarkers for detecting the lymph node status of breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23238818</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-373</Data></Cell>
    <Cell><Data ss:Type="String">Increased serum levels of circulating exosomal microRNA-373 in receptor-negative breast cancer patients.</Data></Cell>
    <Cell><Data ss:Type="String">Serum levels of exosomal miR-373 are linked to triple negative and more aggressive breast carcinomas.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25333260</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-373</Data></Cell>
    <Cell><Data ss:Type="String">Increased serum levels of circulating exosomal microRNA-373 in receptor-negative breast cancer patients.</Data></Cell>
    <Cell><Data ss:Type="String">Overexpression of miR-373 by transfection of MCF-7 cells showed downregulated protein expression of the estrogen receptor, and inhibition of apoptosis induced by camptothecin. Our data indicate that serum levels of exosomal miR-373 are lin</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25333260</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-378d</Data></Cell>
    <Cell><Data ss:Type="String">Exosomes from bulk and stem cells from human prostate cancer have a differential microRNA content that contributes cooperatively over local and pre-metastatic niche</Data></Cell>
    <Cell><Data ss:Type="String">Thirteen miRNAs were overexpressed in exosomes from bulk cells: hsa-miR-218-5p, hsa-miR-7-5p, hsa-miR-1290, hsa-miR-17-5p, hsa-miR-20a-5p, hsa-miR-503-5p, hsa-miR-30c-5p, hsa-miR-125b-1, hsa-miR-21-5p, hsa-miR-93-5p, hsa-miR-378c, hsa-miR-378d and hsa-miR-25-3p</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26675257</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-378d</Data></Cell>
    <Cell><Data ss:Type="String">Genomic characterization of liver metastases from colorectal cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">In turn, the CLCA4, CA1, SLC4A4, AQP8, and ZG16 mRNAs together with the miR-215, miR-139, miR-133a, miR-378c and miR-378d miRNAs were those genes showing the strongest down-regulated levels across all primary tumor samples analyzed</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27662660</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-378e</Data></Cell>
    <Cell><Data ss:Type="String">Identification of microRNA signature and potential pathway targets in prostate cancer</Data></Cell>
    <Cell><Data ss:Type="String">The miRNAs 378e and 378i can potentially target homeobox?NKX-3.1?mRNA and inhibit its selective prostate tumor suppressor activity</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27903835</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-378e</Data></Cell>
    <Cell><Data ss:Type="String">Cancer-associated fibroblasts?release?exosomal?microRNAs that dictate an aggressive phenotype in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Breast cancer cells exposed to CAF exosomes containing miR-21, miR-378e, and miR-143, exhibited a significantly increased capacity to promote stemness properties, EMT phenotype, and anchorage-independent cell growth</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28121625</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-378e</Data></Cell>
    <Cell><Data ss:Type="String">Exosomal microRNA: a novel biomarker for breast?cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-21, miR-378e, miR-143, miR-222, miR-223, miR-16, miR-100, miR-23b, miR-19a and miR-503 from breast stromal cells increased stemness, epithelial-esenchymal transition, brain metastasis, drug resistance, and dormancy and regulated angiogenesis of cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29151358</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-382</Data></Cell>
    <Cell><Data ss:Type="String">Presence of Circulating hsa-miR-145, hsa-miR-155, and hsa-miR-382 in Exosomes Isolated from Serum of Breast Cancer Patients and Healthy Donors</Data></Cell>
    <Cell><Data ss:Type="String">Our study showed that serum-circulating miR-145, miR-155, and miR-382 are present in exosomes. These miRNAs were previously proposed as noninvasive biomarkers to distinguish between BC patients and healthy individuals</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">30891102</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-382</Data></Cell>
    <Cell><Data ss:Type="String">miR-382 inhibits tumor growth and enhance chemosensitivity in osteosarcoma</Data></Cell>
    <Cell><Data ss:Type="String">A novel functional pathway controlled by miR-382 and its direct targets, KLF12 and HIPK3, that coordinate tumor growth and chemosensitivity, respectively, in OS.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25344865</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3922-5p</Data></Cell>
    <Cell><Data ss:Type="String">Identification of dysregulated microRNAs associated with diagnosis and prognosis in triple?negative breast cancer: An in silico study</Data></Cell>
    <Cell><Data ss:Type="String">A 4 miRNA signature consisting of hsa-miR-148b, hsa-miR-203a, hsa-miR-203b and hsa-miR-3922 was constructed for prediction of prognosis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30942465</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3922-5p</Data></Cell>
    <Cell><Data ss:Type="String">miR-1915-3p inhibits Bcl-2 expression in the development of gastric cancer</Data></Cell>
    <Cell><Data ss:Type="String">Previous microRNA microarray results suggest that miR-338-5p, miR-1915-3p, miR-3621, miR-3178 and miR-3196 were down-regulated in MKN-45 cells, whereas the expression of miR-3173-3p, miR-3922-5p and miR-609 were up-regulated</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31036603</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3936</Data></Cell>
    <Cell><Data ss:Type="String">Variation in MicroRNA Expression Profile of Uterine Leiomyoma with Endometrial Cavity Distortion and Endometrial Cavity Non-Distortion</Data></Cell>
    <Cell><Data ss:Type="String">The qRT-PCR results showed that miR-1260b, miR-3936, miR-4267, miR-4638-5p, miR-4695-3p, miR-4734, miR-5096, and miR-8603 were significantly up-regulated in LNG-treated cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="String">?30149651</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3960</Data></Cell>
    <Cell><Data ss:Type="String">MiR-3960 binding sites with mRNA of human genes</Data></Cell>
    <Cell><Data ss:Type="String">MiR-3960 has more than 1000mRNA binding sites with high affinity (with △G/△Gm values greater than or equal to 90%) for 375genes. The miR-3960 has 565 binding sites in the 5'UTRs and 515 sites in theCDS of mRNAs;miR-3960 has binding sites in 73 mRNAs of target genesencoded transcription factors</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25187682</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3960</Data></Cell>
    <Cell><Data ss:Type="String">Runx2/miR-3960/miR-2861 Positive Feedback Loop Is Responsible for Osteogenic Transdifferentiation of Vascular Smooth Muscle Cells</Data></Cell>
    <Cell><Data ss:Type="String">Runx2/miR-3960/miR-2861 positive feedback loop plays an important role in osteogenic transdifferentiation of VSMCs and contributes to vascular calcification</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26221600</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3960</Data></Cell>
    <Cell><Data ss:Type="String">Downregulation of long noncoding RNA HOTAIRM1 promotes monocyte/dendritic cell differentiation through competitively binding to endogenous miR-3960</Data></Cell>
    <Cell><Data ss:Type="String">HOTAIRM1 competitively binds to miR-3960 and finally regulates the process of hematopoiesis, which reveals a novel regulatory mechanism of lncRNA function</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28280365</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-3960</Data></Cell>
    <Cell><Data ss:Type="String">Circulating miRNA panels for specific and early detection in bladder cancer</Data></Cell>
    <Cell><Data ss:Type="String">We found that a combination of 7 miRNA (7-miRNA panel: miR-6087, miR-6724-5p, miR-3960, miR-1343-5p, miR-1185-1-3p, miR-6831-5p and miR-4695-5p) could discriminate bladder cancer from non-cancer and other types of tumors with the highest accuracy</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30382619</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4261</Data></Cell>
    <Cell><Data ss:Type="String">Tumor heterogeneity in the recurrence of epithelial ovarian cancer demonstrated by polycomb group proteins</Data></Cell>
    <Cell><Data ss:Type="String">MiR-4261 and miR-298 had seed match with ZNF207 3'-UTR and ILF3 3'-UTR, and in turn, ZNF207 and ILF3 are transcription factors of EZH2 promoter, suggesting that miR-4261 and miR-298 might indirectly regulate the expression of EZH2 through intermediate factors</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25285018</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4261</Data></Cell>
    <Cell><Data ss:Type="String">Therapeutic Suppression of miR-4261 Attenuates Colorectal Cancer by Targeting MCC</Data></Cell>
    <Cell><Data ss:Type="String">Inhibition of miR-4261 through targeting of MCC might exert a therapeutic effect for colorectal cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28918036</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4261</Data></Cell>
    <Cell><Data ss:Type="String">Downregulated MEG3 contributes to tumour progression and poor prognosis in oesophagal squamous cell carcinoma by interacting with miR-4261, downregulating DKK2 and activating the Wnt/β-catenin signalling</Data></Cell>
    <Cell><Data ss:Type="String">Our study for the first time elaborated the critical role of MEG3-miR-4261-DKK2-Wnt/β-catenin signalling axis in ESCC, and MEG3 could represent a novel diagnostic and prognostic biomarker and therapeutic target in ESCC</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30990378</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4269</Data></Cell>
    <Cell><Data ss:Type="String">Long noncoding intronic RNAs are differentially expressed in primary and metastatic pancreatic cancer</Data></Cell>
    <Cell><Data ss:Type="String">We found four putative extended EST sequences that show high similarity to seven additional small RNAs: hsa-mir-1259, hsa-mir-326, hsa-mir-4269, hsa-mir-675, SNORD12, SNORD12B and SNORD12C</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22078386</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4269</Data></Cell>
    <Cell><Data ss:Type="String">TEAD1/4 exerts oncogenic role and is negatively regulated by miR-4269 in gastric tumorigenesis</Data></Cell>
    <Cell><Data ss:Type="String">The nuclear accumulated TEAD4 and downregulated miR-4269 are proposed to serve as novel prognostic biomarkers in GC</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28759040</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4269</Data></Cell>
    <Cell><Data ss:Type="String">TEAD1/4 exerts oncogenic role and is negatively regulated by miR-4269 in gastric tumorigenesis</Data></Cell>
    <Cell><Data ss:Type="String">Downregulation of miR-4269 was associated with poor disease-specific survival and showed a negative correlation with TEAD4</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28759040</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4269</Data></Cell>
    <Cell><Data ss:Type="String">Targeting BTK through microRNA in chronic lymphocytic leukemia</Data></Cell>
    <Cell><Data ss:Type="String">A set of six miRNAs predicted to target BTK with high specificity by several algorithms (miR-147b, miR-210, miR-425, miR-1253, miR-4269, and miR-4667-3p) substantially decreased BTK expression in Mec2 cell lines derived from CLL patients</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="String">?27756747</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4271</Data></Cell>
    <Cell><Data ss:Type="String">When the T minor allele is present in the cell, miR-4271 is able to bind to the 3'UTR of APOC3, and this leads to a decreased translation of APOC3</Data></Cell>
    <Cell><Data ss:Type="String">When the T minor allele is present in the cell, miR-4271 is able to bind to the 3'-UTR of APOC3, and this leads to a decreased translation of APOC3</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28381629</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4277</Data></Cell>
    <Cell><Data ss:Type="String">Identification of chemoresistance-associated miRNAs in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Expression levels of miR-3617-3p, miR-3136-3p, miR-4277, and miR-92a-1-5p in Bats-72 cell were obviously much higher than the Bcap37 cell, whereas miR-520b was significantly downregulated in the Bats-72 cell?</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30425571</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4278</Data></Cell>
    <Cell><Data ss:Type="String">SNP rs3202538 in 3'UTR region of ErbB3 regulated by miR-204 and miR-211 promote gastric cancer development in Chinese population</Data></Cell>
    <Cell><Data ss:Type="String">Further genotyping was performed to detect the distribution of allele gene of the SNP in our research, among all this SNPs, rs3202538 which can be potentially regulated by miR-204 miR-211 and miR-4278 were in Hardy-Heinberg equilibrium distribution pattern in the healthy control group (P?&lt;?0.0001)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28924391</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4278</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-4728 serves as a suppressor and antagonist of oncogenic MAPK in Burkitt lymphoma</Data></Cell>
    <Cell><Data ss:Type="String">MiR-4728 serves as a suppressor and antagonist of oncogenic MAPK in Burkitt lymphoma. The appropriate regulation of miR-4728 might be vital to improve BL treatment</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="String">?30108451</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4280</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA signature of breast cancer brain metastasis for novel targeted therapies</Data></Cell>
    <Cell><Data ss:Type="String">The upregulated miRNAs included miR-3927-5p, miR-216b and miR-10b and the down regulated miRNAs were miR-4280, miR-3174 and miR-1244 and miR20b</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4294</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA Markers for the Diagnosis of Pancreatic and Biliary-Tract Cancers</Data></Cell>
    <Cell><Data ss:Type="String">MiR-6075, miR-4294, miR-6880-5p, miR-6799-5p, miR-125a-3p, miR-4530, miR-6836-3p, and miR-4476suggested as early diagnostic biomarkers to detect pancreatobiliary cancers </Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25706130</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4298</Data></Cell>
    <Cell><Data ss:Type="String">Identification of microRNAs Specifically Expressed in Hepatitis C Virus-Associated Hepatocellular Carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">Four (miR-4298, miR-575, miR-33b-3p and mir-610_x) and two (mir-517a_x, miR-21-3p) miRNAs were found to be exclusively expressed by liver donors and normal livers, respectively</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23390000</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4298</Data></Cell>
    <Cell><Data ss:Type="String">MiR-23a in amplified 19p13.13 loci targets metallothionein 2A and promotes growth in gastric cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">We identified eight miRNAs (miR-1274a, miR-196b, miR-4298, miR-181c, miR-181d, miR-23a, miR-27a and miR-24-2) that were located in the amplified regions and were upregulated in GC</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23553990</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4298</Data></Cell>
    <Cell><Data ss:Type="String">Low serum level of miR-485-3p predicts poor survival in patients with glioblastoma</Data></Cell>
    <Cell><Data ss:Type="String">No significant correlation was found between survival rates (PFS and OS) and the expression levels of miR-451a and miR-4298 in GBM patients</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28931080</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4298</Data></Cell>
    <Cell><Data ss:Type="String">Low serum level of miR-485-3p predicts poor survival in patients with glioblastoma</Data></Cell>
    <Cell><Data ss:Type="String">Based on the profiling result of serum miRNAs in GBM patients, we first carried out qRT-PCR on 3 miRNAs (miR-451a, miR-485-3p and miR-4298) in an new cohort (24 GBM patients and 12 healthy volunteers) to validate the microarray data</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28931080</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4324</Data></Cell>
    <Cell><Data ss:Type="String">Identification of circulating microRNA signatures for breast?cancer?detection</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNAs that were upregulated (miR-720, miR1274b and miR-1260), or downregulated (miR-30c, miR-376c and miR-4324), in breast cancer tumours will be likely candidates for novel oncomirs or tumor suppressors, respectively</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23797906</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4324</Data></Cell>
    <Cell><Data ss:Type="String">A Panel of MicroRNA Signature as a Tool for Predicting Survival of Patients with Urothelial Carcinoma of the Bladder</Data></Cell>
    <Cell><Data ss:Type="String">Of nine miRNAs, six were associated with high risk (hsa-miR-99a-5p, hsa-miR-100-5p, hsa-miR-125b-5p, hsa-miR-4324, hsa-miR-34b-5p, and hsa-miR-135a-3p) and three were shown to be protective (hsa-miR-145-5p, hsa-miR-29c-3p, and hsa-miR-33b-3p</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30026881</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4440</Data></Cell>
    <Cell><Data ss:Type="String">Genomic characterization of liver metastases from colorectal cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">Newly deregulated metastatic transcripts included overexpression of APOA1, HRG, UGT2B4, RBP4 and ADH4 mRNAS and the miR-3180-3p, miR-3197, miR-3178, miR-4793 and miR-4440 miRNAs, together with decreased expression of the IGKV1-39, IGKC, IGKV1-27, FABP4 and MYLK mRNAS and the miR-363, miR-1, miR-143, miR-27b and miR-28-5p miRNAs</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27662660</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4443</Data></Cell>
    <Cell><Data ss:Type="String">miR-4443 Participates in the Malignancy of Breast Cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-4443 induced malignancy of breast cancer mainly in chemo-resistance aspect for the very first time, providing a novel biomarker in breast cancer diagnosis and therapy</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27504971</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4443</Data></Cell>
    <Cell><Data ss:Type="String">Leptin and insulin up-regulate miR-4443 to suppress NCOA1 and TRAF4, and decrease the invasiveness of human colon cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">MiR-4443 acts in a tumor-suppressive manner by down-regulating TRAF4 and NCOA1 downstream of MEK-C/EBP-mediated leptin and insulin signaling, and that insulin and/or leptin resistance (e.g. in obesity) may suppress this pathway and increase the risk of metastatic CRC</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27842582</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4443</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-4443 Causes CD4+ T Cells Dysfunction by Targeting TNFR-Associated Factor 4 in Graves Disease</Data></Cell>
    <Cell><Data ss:Type="String">The increased expression of miR-4443 induced CD4+ T cells dysfunction by targeting TRAF4, which may cause GD</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29163513</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4443</Data></Cell>
    <Cell><Data ss:Type="String">Downregulation of miR-4443 and miR-5195-3p in ovarian cancer tissue contributes to metastasis and tumorigenesis</Data></Cell>
    <Cell><Data ss:Type="String">Further investigation can help to suggest miR-4443 and miR-5195-3p as diagnostic biomarkers or therapeutic targets in OC</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30810880</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4443</Data></Cell>
    <Cell><Data ss:Type="String">Downregulation of miR-4443 and miR-5195-3p in ovarian cancer tissue contributes to metastasis and tumorigenesis</Data></Cell>
    <Cell><Data ss:Type="String">MiR-4443 and miR-5195-3p may contribute to suppressing tumor, so that decrease in their expression is associated with increased cell proliferation and invasion</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30810880</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4443</Data></Cell>
    <Cell><Data ss:Type="String">CircASS1 suppressed the invasion and metastasis ability of breast cancer cell line by targeting gene ASS1 and harboring miR-4443</Data></Cell>
    <Cell><Data ss:Type="String">CircASS1 suppresses invasion and migration capacity of BC cells by increasing expression of ASS1 and circASS1 could harbor miR-4443, suggesting that circASS1 could be a potential target in BC treatment and a prospective prognostic biological marker in BC.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4445-3p</Data></Cell>
    <Cell><Data ss:Type="String">miR-4324-RACGAP1-STAT3-ESR1 feedback loop inhibits proliferation and metastasis of bladder?cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-4324-RACGAP1-STAT3-ESR1 feedback loop could be a critical regulator of BCa progression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30511377</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4451</Data></Cell>
    <Cell><Data ss:Type="String">Overexpression of miRNA 4451 is Associated With a Poor Survival of Patients With Hypopharyngeal Cancer After Surgery With Postoperative Radiotherapy</Data></Cell>
    <Cell><Data ss:Type="String">Upregulated miR-4451 in HC samples were frequently found and is significantly associated with advanced stage and poor survival of HC, which may indicate an association of this miRNA with the carcinogenesis process in this tumor site; and they could serve as a prognostic biomarker as well as help develop potential new targets for therapy</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30103154</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4462</Data></Cell>
    <Cell><Data ss:Type="String">Mitochondrial miRNA Determines Chemoresistance by Reprogramming Metabolism and Regulating Mitochondrial Transcription</Data></Cell>
    <Cell><Data ss:Type="String">Meanwhile, some other mitomiRs, including miR-371a-5p, miR-4271, miR-4462, miR-1290, and miR-4449, had no effect on apoptosis in both TSCC cell lines</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4470</Data></Cell>
    <Cell><Data ss:Type="String">Association of cigarette smoking and microRNA expression in rectal cancer: Insight into tumor phenotype</Data></Cell>
    <Cell><Data ss:Type="String">Ten miRNAs (hsa-miR-1914-3p, hsa-miR-4327, hsa-miR-4470, hsa-miR-4665-3p, hsa-miR-4673, hsa-miR-548q, hsa-miR-550b-2-5p, hsa-miR-6074, hsa-miR-6165, and hsa-miR-939-5p) were upregulated in tumors of rectal cases of current smokers and the differential expression of these miRNAs was previously shown to be associated with worse survival when expression in carcinoma tissue increased</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27780077</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4497</Data></Cell>
    <Cell><Data ss:Type="String">Analysis of the miRNA Profiles of Melanoma Exosomes Derived Under Normoxic and Hypoxic Culture Conditions</Data></Cell>
    <Cell><Data ss:Type="String">Comparing miRNA profiles in exosomes derived from melanoma cells grown at high (21%) and low (1%) concentrations of oxygen revealed that 15 miRNAs were significantly more abundant under hypoxic conditions, with miR-494, miR-6087, miR-513a, and miR-4497 being the most dramatically enriched</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29187456</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4497</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-4497 functions as a tumor suppressor in laryngeal squamous cell carcinoma via negatively modulation the GBX2.</Data></Cell>
    <Cell><Data ss:Type="String">MiR-4497 may play a suppressive role in LSCC by targeting GBX2, which offer new insights into the tumorigenesis of LSCC</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29843929</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4529-3p</Data></Cell>
    <Cell><Data ss:Type="String">miRNome landscape analysis reveals a 30 miRNA core in retinoblastoma</Data></Cell>
    <Cell><Data ss:Type="String">MiR-16 as present and miR-4529-3p as absent using qRT-PCR as part of our initial approach to describe the general miRNOME landscape of miRNAs in the on/off state</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28668075</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4539</Data></Cell>
    <Cell><Data ss:Type="String">Expression Profiles of miRNA Subsets Distinguish Human Colorectal Carcinoma and Normal Colonic Mucosa</Data></Cell>
    <Cell><Data ss:Type="String">We identified 16 miRNAs for colon and 17 miRNAs for rectal carcinoma that appear to differentiate between carcinoma and normal mucosa; of these, 12 were important for both colon and rectal cancer, hsa-miR-663b, hsa-miR-4539, hsa-miR-17-5p, hsa-miR-20a-5p, hsa-miR-21-5p, hsa-miR-4506, hsa-miR-92a-3p, hsa-miR-93-5p, hsa-miR-145-5p, hsa-miR-3651, hsa-miR-378a-3p, and hsa-miR-378i</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26963002</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4539</Data></Cell>
    <Cell><Data ss:Type="String">Comprehensive circular RNA profiling identifies CircFAM120A as a new biomarker of hypoxic lung adenocarcinoma</Data></Cell>
    <Cell><Data ss:Type="String">According to this network, the top six predicted miRNA targets of each differentially expressed circRNAs were hsa-miR-12119, hsa-miR-370-3p, hsa-miR-370-3p, hsa-miR-4539, hsa-miR-6511a-5p, hsa-miR-6772-3p and hsa-miR-9851-3p</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28710406</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4656</Data></Cell>
    <Cell><Data ss:Type="String">Identification of dysregulated miRNAs and their regulatory signature in glioma patients using the partial least squares method</Data></Cell>
    <Cell><Data ss:Type="String">The expression levels of hsa-miR-1908, hsa-miR-4656 and hsa-miR-4680 have been identified to significantly correlate with the survival rate</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25452796</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4656</Data></Cell>
    <Cell><Data ss:Type="String">Transcriptome-wide analysis of compression-induced microRNA expression alteration in breast cancer for mining therapeutic targets</Data></Cell>
    <Cell><Data ss:Type="String">The most downregulated target mRNA was TSPAN7, a putative target of miR-4656</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27027350</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4656</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-4656 is a prognostic factor and tumor suppressor in human pancreatic cancer through a downstream target of TrkA</Data></Cell>
    <Cell><Data ss:Type="String">MiR-4656 is expressed to a low extent and is a potential biomarker in PC</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27936486</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4656</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-4656 is a prognostic factor and tumor suppressor in human pancreatic cancer through a downstream target of TrkA</Data></Cell>
    <Cell><Data ss:Type="String">Overexpressing miR-4656 has tumor suppressive effects on PC development both in vitro and in vivo, likely through its downstream target of the TrkA gene</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27936486</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-466</Data></Cell>
    <Cell><Data ss:Type="String">A New MicroRNA Expression Signature for Cervical Cancer</Data></Cell>
    <Cell><Data ss:Type="String">The aberrant expression of miR-466 is closely associated with the occurrence and development of cervical cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27870701</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-466</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-466 inhibits tumor growth and bone metastasis in prostate cancer by direct regulation of osteogenic transcription factor RUNX2</Data></Cell>
    <Cell><Data ss:Type="String">MiR-466-mediated attenuation of RUNX2 as a novel therapeutic approach to regulate PCa growth, particularly metastasis to bone</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28125091</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-466</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-466 (miR-466) functions as a tumor suppressor and prognostic factor in colorectal cancer (CRC)</Data></Cell>
    <Cell><Data ss:Type="String">MiR-466 functions as a suppressor miRNA in CRC and may be used as a prognostic factor in these patients</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29338680</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-466</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-466 (miR-466) functions as a tumor suppressor and prognostic factor in colorectal cancer (CRC)</Data></Cell>
    <Cell><Data ss:Type="String">MiR-466 suppressed cell proliferation and migration/invasion, as well as induced G0/G1 arrest and apoptosis in SW-620 cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29338680</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-466</Data></Cell>
    <Cell><Data ss:Type="String">CREB1 induced lncRNA HAS2-AS1 promotes epithelial ovarian cancer proliferation and invasion via the miR-466/RUNX2 axis</Data></Cell>
    <Cell><Data ss:Type="String">The CREB1/HAS2-AS1/miR-466/RUNX2 axis in the in the EOC tumorigenesis, providing the novel insight for the molecular mechanism of EOC</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31082772</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-466</Data></Cell>
    <Cell><Data ss:Type="String">HPV E6/E7 oncoprotein promotes cervical cancer by promoting miR-466 expression via P53 pathway</Data></Cell>
    <Cell><Data ss:Type="String">HPV E6/E7 oncoprotein probably promotes miRNA-466 expression via P53 pathway</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4669</Data></Cell>
    <Cell><Data ss:Type="String">Novel circulating microRNAs expression profile in colon cancer: a pilot study</Data></Cell>
    <Cell><Data ss:Type="String">Clinical analysis of miR-31, miR-141, miR-224-3p, miR-576-5p, and miR-4669 expression in patients with colon cancer may facilitate the diagnosis of colon cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29187262</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4674</Data></Cell>
    <Cell><Data ss:Type="String">Cell-specific post-transcriptional regulation of γ-synuclein gene by micro-RNAs</Data></Cell>
    <Cell><Data ss:Type="String">Expression of miR-4437 and miR-4674 for which putative targets in 3'-UTR were predicted caused a 61.2% and 60.1% reduction of endogenous γ-synuclein expression confirming their role in gene expression regulation</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24040069</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4674</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA hsa-miR-4674 in Hemolysis-Free Blood Plasma Is Associated with Distant Metastases of Prostatic Cancer</Data></Cell>
    <Cell><Data ss:Type="String">The metastatic form of prostatic cancer was found to be associated with increased levels of hsa-miR-22-3p, hsa-miR-663a, and hsa-miR-4674 in comparison with non-metastatic form. Common candidate target genes of these microRNA include JUNB, KMT2A, and XPO6</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27265126</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4674</Data></Cell>
    <Cell><Data ss:Type="String">miR-596 Modulates Melanoma Growth by Regulating Cell Survival and Death</Data></Cell>
    <Cell><Data ss:Type="String">We found that the 8p23.3 locus contains not only miR-596, but also miR-4674 and miR-7160</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29183729</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4684-3p</Data></Cell>
    <Cell><Data ss:Type="String">Genetic variants in the TGFβ-signaling pathway influence expression of miRNAs in colon and rectal normal mucosa and tumor tissue</Data></Cell>
    <Cell><Data ss:Type="String">MiR-4684-3p was upregulated in the variant allele of NFκB1 rs230510 while downregulated in the presences of the variant allele of NFκB1 rs3821958</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28061442</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4689</Data></Cell>
    <Cell><Data ss:Type="String">Concurrent Targeting of KRAS and AKT by MiR-4689 Is a Novel Treatment Against Mutant KRAS Colorectal Cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-4689 may be a promising therapeutic agent in mutant KRAS CRC</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25756961</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4689</Data></Cell>
    <Cell><Data ss:Type="String">Concurrent Targeting of KRAS and AKT by MiR-4689 Is a Novel Treatment Against Mutant KRAS Colorectal Cancer</Data></Cell>
    <Cell><Data ss:Type="String">Mutant KRAS functions as a broad regulator of the EGFR signaling cascade by inhibiting miR-4689, which negatively regulates both RAS/mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K)/AKT pathways</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25756961</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4689</Data></Cell>
    <Cell><Data ss:Type="String">Serum microRNA microarray analysis identifies miR-4429 and miR-4689 are potential diagnostic biomarkers for biliary atresia</Data></Cell>
    <Cell><Data ss:Type="String">Differentially expressed miRNAs including hsa-miR-4429 and hsa-miR-4689 might play critical roles in BA by regulating their target genes, and these two miRNAs may have the potential to become diagnostic biomarkers</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26879603</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4692</Data></Cell>
    <Cell><Data ss:Type="String">The Pharmacological Effects of Spatholobi Caulis Tannin in Cervical Cancer and Its Precise Therapeutic Effect on Related circRNA.</Data></Cell>
    <Cell><Data ss:Type="String">The RegRNA analysis led to the following predictions: circE2F3 binds hsa-miR-211-5p, hsa-miR-4459, hsa-miR-3960, hsa-miR-4632, hsa-miR-4739, and hsa-miR-5006-3p and circFANCB binds hsa-miR-4692</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31194163</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4716-3p</Data></Cell>
    <Cell><Data ss:Type="String">The Sequence and Structure Determine the Function of Mature Human miRNAs</Data></Cell>
    <Cell><Data ss:Type="String">MiR-4290, miR-1281, miR-4716-5p, miR-483-3p and miR-877-3p containing almost only UC nucleotides and miR-6124, miR-483-5p, miR-4271, miR-4644, miR-4716-3p and miR-1234-5p purine-rich</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27031951</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4723-5p</Data></Cell>
    <Cell><Data ss:Type="String">Genome-wide MicroRNA Expression Profiles in COPD: Early Predictors for Cancer Development</Data></Cell>
    <Cell><Data ss:Type="String">We found that expression of 19 miRNAs, most strongly miR-4723-5p, was significantly correlated with the 6-min walk distance following adjustment for multiple testing</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29981854</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4723-5p</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA 4723-5p is novel tumor suppressor microRNA in prostate cancer that directly regulates Abelson family of nonreceptor protein tyrosine kinases</Data></Cell>
    <Cell><Data ss:Type="String">MiR-4723-5p may be an attractive target for therapeutic intervention in prostate cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4726-5p</Data></Cell>
    <Cell><Data ss:Type="String">Circular RNA Expression Profile in Laryngeal Squamous Cell Carcinoma Revealed by Microarray</Data></Cell>
    <Cell><Data ss:Type="String">Competitive endogenous RNA network prediction and bioinformatics functional analysis revealed that hsa_circ_0044520 and hsa_circ_0044529 play important regulatory roles by sponging hsa-miR-4726-5p and hsa-miR-4640-5p, thereby providing novel insights into the tumorigenesis of LSCC</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30282067</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4732-5p</Data></Cell>
    <Cell><Data ss:Type="String">miR-144/451 cluster plays an oncogenic role in esophageal cancer by inhibiting cell invasion</Data></Cell>
    <Cell><Data ss:Type="String">MiR-144-3p, miR-451a, miR-4732-3p and miR-4732-5p inhibited cell migration</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21199797</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4732-5p</Data></Cell>
    <Cell><Data ss:Type="String">Identification of New MicroRNAs in Paired Normal and Tumor Breast Tissue Suggests a Dual Role for the?ERBB2/Her2?Gene</Data></Cell>
    <Cell><Data ss:Type="String">Two of the 5, miR-3150b-3p and miR-4732-5p, were not detected in any other tissue, suggesting that they may be specific to breast</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21199797</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4732-5p</Data></Cell>
    <Cell><Data ss:Type="String">Overlapping region of p53/wrap53 transcripts: mutational analysis and sequence similarity with microRNA-4732-5p</Data></Cell>
    <Cell><Data ss:Type="String">By binding with the 5'-untranslated region of WRAP53, hsa-miR-4732-5p promoted breast cancer progression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23886136</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4732-5p</Data></Cell>
    <Cell><Data ss:Type="String">Relapse-associated microRNA in gastric cancer patients after S-1 adjuvant chemotherapy</Data></Cell>
    <Cell><Data ss:Type="String">MiR-92b, miR?422a, miR-4732-5p and miR-4758-3p are closely associated with relapse following S-1 adjuvant chemotherapy in gastric cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24317477</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4732-5p</Data></Cell>
    <Cell><Data ss:Type="String">Bioinformatics analysis of dysregulated microRNAs in the nipple discharge of patients with breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">The predicted target genes of miR-3646, -4484 and -4732-5p were identified to serve a role in cancer-associated signaling pathways and TF-mRNA networks, indicating that they serve a role in breast carcinogenesis and progression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28521415</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4732-5p</Data></Cell>
    <Cell><Data ss:Type="String">miR-732-p promotes breast cancer progression by targeting TSPAN13</Data></Cell>
    <Cell><Data ss:Type="String">MiR-4732-5p may serve as a tumour suppressor in the initiation of breast cancer, but as a tumour promoter in breast cancer progression by targeting TSPAN13</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30701690</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4745-5p</Data></Cell>
    <Cell><Data ss:Type="String">Novel miRNAs as potential biomarkers in stage II colon cancer: microarray analysis</Data></Cell>
    <Cell><Data ss:Type="String">Of 32 identified miRNAs, an increase in three microRNAs (hsa-miR-4745-5p, hsa-miR-6126, and hsa-miR-1469) was observed in tumor tissues relative to that in control tissues</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31123908</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4778-5p</Data></Cell>
    <Cell><Data ss:Type="String">miRNA expression patterns in normal breast tissue and invasive breast cancers of BRCA1 and BRCA2 germ-line mutation carriers</Data></Cell>
    <Cell><Data ss:Type="String">MiR-4778-5p, miR-4433, miR-5010-5p, miR-1287, miR-663b, and miR-4688 (up-regulated in BRCA2-associated breast carcinomas compared to their normal counterparts, and not consequently deregulated in sporadic breast carcinomas);</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26378051</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-4790-3p</Data></Cell>
    <Cell><Data ss:Type="String">Identification of microRNA signature and potential pathway targets in prostate cancer</Data></Cell>
    <Cell><Data ss:Type="String">The endogenous levels of miR-30d-5p, 603, 363-3p, 3120, 1299, let-7b-5p, and 200a-3p were found to be downregulated, whereas those of miR-4790-3p, 1305, 19a-3p, and 548 were found to be upregulated in C4-2B cells compared to RWPE-1 cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="String">?27903835</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-486-5p</Data></Cell>
    <Cell><Data ss:Type="String">Differential expression of exosomal miRNAs between breast cancer patients with and without recurrence</Data></Cell>
    <Cell><Data ss:Type="String">Of 384 miRNAs, three miRNAs (miR-338-3p, miR-340-5p, and miR-124-3p) were significantly upregulated and eight (miR-29b-3p, miR-20b-5p, miR-17-5p, miR-130a-3p, miR-18a-5p, miR-195-5p, miR-486-5p, and miR-93-5p) were significantly downregulated in the patients with recurrence</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29050253</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-486-5p</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-486-5p targeting PIM-1 suppresses cell proliferation in breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">MiR-486-5p/PIM-1 axis provides insight into the pathogenesis of BC and might be therapeutic targets for prevention or treatment of BC</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25104088</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-486-5p</Data></Cell>
    <Cell><Data ss:Type="String">Down-regulated miR-486-5p acts as a tumor suppressor in breast cancer patients by targeting the metastatic mediator ICAM-1</Data></Cell>
    <Cell><Data ss:Type="String">MiR-486-5p decreases the metastatic property of ICAM-1. In addition, miR-486-5p acts as a tumor suppressor in BC;increasing the levels of the under-expressed miR-486-5p in TNBC tissues can be a possible therapeutic approach for halting BC progression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27882172</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-486-5p</Data></Cell>
    <Cell><Data ss:Type="String">S-Adenosylmethionine regulates apoptosis and autophagy in MCF-7 breast cancer cells through the modulation of specific microRNAs</Data></Cell>
    <Cell><Data ss:Type="String">MiR-486-5p inhibitor induces autophagy and enhances AdoMet-induced autophagic process by increasing PTEN expression and by inhibiting AKT signaling</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30533999</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-486-5p</Data></Cell>
    <Cell><Data ss:Type="String">MiR-486-5p prevents migration, invasion and EMT by regulating Smad2 in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-486-5p may represent as a new treatment target and prognostic marker for breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-5001-5p</Data></Cell>
    <Cell><Data ss:Type="String">Tissue-specific and plasma microRNA profiles could be promising biomarkers of histological classification and TNM stage in non-small cell lung cancer</Data></Cell>
    <Cell><Data ss:Type="String">15 specific plasma miRNAs, let-7d-3p,miR-106b-5p,miR-144-3p,miR-197-3p,miR-19b3p, miR-211-3p, miR-30e-5p, miR-345-3p, miR-3679-3p, miR-423-5p, miR-451a, miR-4787-5p, miR-5001-5p, miR5100 and miR-6068, could be promising biomarkers of lung squamous cell carcinoma, and nine specific plasma miRNA</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27148421</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-5001-5p</Data></Cell>
    <Cell><Data ss:Type="String">Identification of MicroRNAs Involved in Growth Arrest and Apoptosis in Hydrogen Peroxide-Treated Human Hepatocellular Carcinoma Cell Line HepG2</Data></Cell>
    <Cell><Data ss:Type="String">The top six miRNAs were hsa-miR-4763-3p, hsa-miR-149-3p, hsa-miR-762, hsa-miR-5001-5p, hsa-miR-5787, and hsa-miR-6791-5p, while the top six target genes were CPLX2, ZNF385A, NFIX, CNIH2, SOX12, and WDTC1</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27597883</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-503</Data></Cell>
    <Cell><Data ss:Type="String">Endothelial exosomes contribute to the antitumor response during breast cancer neoadjuvant chemotherapy via microRNA transfer</Data></Cell>
    <Cell><Data ss:Type="String">Our data are the first to reveal the involvement of the endothelium in the modulation of tumor development via the secretion of circulating miR-503 in response to chemotherapy treatment</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">25860935</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-503</Data></Cell>
    <Cell><Data ss:Type="String">miR-503 represses human cell proliferation and directly targets the oncogene DDHD2 by non-canonical target pairing</Data></Cell>
    <Cell><Data ss:Type="String">MiR-503 may act as a tumor suppressor in breast cancer by its direct non-canonical targeting of DDHD2</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25653011</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-503</Data></Cell>
    <Cell><Data ss:Type="String">MiR-503 inhibited cell proliferation of human breast cancer cells by suppressing CCND1 expression</Data></Cell>
    <Cell><Data ss:Type="String">Our findings provide new knowledge regarding the role of miR-503 in the progression of breast cancer and indicate the role of miR-503 as a tumor suppressor microRNA (miRNA) in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26047605</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-503</Data></Cell>
    <Cell><Data ss:Type="String">miR-503-3p promotes epithelial-mesenchymal transition in breast cancer by directly targeting SMAD2 and E-cadherin</Data></Cell>
    <Cell><Data ss:Type="String">Our findings support a critical role for miR-503-3p in induction of breast cancer EMT and suggest that plasma miR-503-3p may be a useful diagnostic biomarker for breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28161325</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-503</Data></Cell>
    <Cell><Data ss:Type="String">miR-424(322)/503 is a breast cancer tumor suppressor whose loss promotes resistance to chemotherapy</Data></Cell>
    <Cell><Data ss:Type="String">MiR-424(322)/503 as a tumor suppressor in breast cancer and provide a link between mammary epithelial involution, tumorigenesis, and the phenomenon of chemoresistance</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28404630</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-5088-5p</Data></Cell>
    <Cell><Data ss:Type="String">MiR-630 acts as a tumor suppressor in cervical cancer and inhibits epithelial-mesenchymal transition in cervical cancer</Data></Cell>
    <Cell><Data ss:Type="String">8 miRNAs genes including miR-5194, miR-5088-5p, miR-192- 5p, miR-331-5p, miR-183-3p were down-regulated in both cell lines </Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-5091</Data></Cell>
    <Cell><Data ss:Type="String">Identification of two microRNA signatures in whole blood as novel biomarkers for diagnosis of nasopharyngeal carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">MiR-5091, miR-513b are promising biomarkers for NPC diagnosis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31159814</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-5091</Data></Cell>
    <Cell><Data ss:Type="String">Genome-scale analysis to identify prognostic microRNA biomarkers in patients with early stage pancreatic ductal adenocarcinoma after pancreaticoduodenectomy</Data></Cell>
    <Cell><Data ss:Type="String">The following 11 prognostic miRNAs were used for the construction of the prognostic signature: hsa-mir-501, hsa-mir-4521, hsa-mir-5091, hsa-mir-24-1, hsa-mir-126, hsa-mir-30e, hsa-mir-3157, hsa-let-7a-3, hsa-mir-133a-1, hsa-mir-4709, and hsa-mir-421</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="String">?30127641</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-5091</Data></Cell>
    <Cell><Data ss:Type="String">Profiling of plasma circulating miRNA in coronary heart disease patients detected by next-generation small RNA sequencing</Data></Cell>
    <Cell><Data ss:Type="String">Five miRNAs were differentially expressed, miR-30c-2-3p and miR-5091 were upregulated and miR-125b-5p, miR501-3p, and miR-31-5p downregulated in plasma of patients with coronary heart disease than in controls</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-583</Data></Cell>
    <Cell><Data ss:Type="String">Circulating miR-583 and miR-663 Refer to ZHENG Differentiation in Chronic Hepatitis B</Data></Cell>
    <Cell><Data ss:Type="String">MiR-583 and miR-663 may be potential markers for ZHENG differentiation in CHB;ROC curve analysis revealed that miR-583 and miR-663 were sensitive and specific enough to distinguish LGDHS from LKYDS</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23554832</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-593-5p</Data></Cell>
    <Cell><Data ss:Type="String">Regulation of cell proliferation and metastasis by microRNA-593-5p in human gastric cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-593-5p inhibited cell proliferation, migration, and invasion and also arrested cell cycle at the G0/G1 phase in SGC-7901 and MGC-803 cells in vitro</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30425531</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-595</Data></Cell>
    <Cell><Data ss:Type="String">Sox17 inhibits hepatocellular carcinoma progression by downregulation of KIF14 expression</Data></Cell>
    <Cell><Data ss:Type="String">IL-22 induces miR-595 expression in papillary thyroid carcinoma, which, in turn, promotes migration and invasion by targeting Sox17, a member of the SRY-related?high-mobility group?(HMG)-box transcription factor superfamily that modulates proliferation, differentiation, migration and invasion in cancers</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25106407</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-595</Data></Cell>
    <Cell><Data ss:Type="String">Circulating microRNAs, miR-939, miR-595, miR-519d and miR-494, Identify Cirrhotic Patients with HCC</Data></Cell>
    <Cell><Data ss:Type="String">Circulating microRNAs deserve attention as non-invasive biomarkers in the diagnostic setting of HCC and that exosomal secretion contributes to discharging a subset of microRNAs into the extracellular compartment</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26509672</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-595</Data></Cell>
    <Cell><Data ss:Type="String">MiR-595 targeting regulation of SOX7 expression promoted cell proliferation of human glioblastoma</Data></Cell>
    <Cell><Data ss:Type="String">MiR-595 expression was significantly upregulated could promote cell proliferation by targeting SOX7</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27133048</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-595</Data></Cell>
    <Cell><Data ss:Type="String">Mir-595 is a significant indicator of poor patient prognosis in epithelial ovarian cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-595 expression might be a novel potential prognostic biomarker for EOC</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29077170</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-595</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-595 sensitizes ovarian cancer cells to cisplatin by targeting ABCB1</Data></Cell>
    <Cell><Data ss:Type="String">MiR-595 acted a tumor suppressor role in ovarian cancer development and increased the sensitivity of ovarian cancer to cisplatin</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="String">?27893429</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-605-3p</Data></Cell>
    <Cell><Data ss:Type="String">Identification of colorectal cancer-restricted microRNAs and their target genes based on high-throughput sequencing data</Data></Cell>
    <Cell><Data ss:Type="String">A total of eight common miRNAs (miRNA-1, miRNA-1265, miRNA-133a-3p, miRNA-133a-5p, miRNA-133b, miRNA-338-3p, miRNA-497-5p, and miRNA-605-3p) were found in tumor and metastasis tissues compared with normal tissues</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27069368</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-605-3p</Data></Cell>
    <Cell><Data ss:Type="String">Circular RNA circ-VANGL1 as a competing endogenous RNA contributes to bladder cancer progression by regulating miR-605-3p/VANGL1 pathway</Data></Cell>
    <Cell><Data ss:Type="String">Our study demonstrated circ-VANGL1/miR-605-3p/VANGL1 as a novel essential signaling pathway involved in BC progression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30146736</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-6068</Data></Cell>
    <Cell><Data ss:Type="String">Urinary exosomal miRNA signature in type II diabetic nephropathy patients</Data></Cell>
    <Cell><Data ss:Type="String">Sixteen urinary exosomal miRNAs were reported to be differentially regulated in a small cohort of T2DKD compared to healthy controls, although only two miRNAs were validated in subsequent replication (miR-320c and miR-6068)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26930277</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-6068</Data></Cell>
    <Cell><Data ss:Type="String">Exosomal transfer of tumor-associated macrophage derived miR-6068 promote ovarian cancer progression</Data></Cell>
    <Cell><Data ss:Type="String">MiR-6068 has an oncogenic role in ovarian cancer progression by targeting PTPN4 and may be a novel effective therapeutic target for ovarian cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-6090</Data></Cell>
    <Cell><Data ss:Type="String">Discovery and Characterization of Novel MicroRNAs During Endothelial Differentiation of Human Embryonic Stem Cells</Data></Cell>
    <Cell><Data ss:Type="String">The expression of 5 miRNAs, specifically hsa-miR-6086, hsa-miR-6087, hsa-miR-6088, hsa-miR-6089 and hsa-miR-6090, were specifically downregulated during endothelial differentiation of human ES cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22142236</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-6090</Data></Cell>
    <Cell><Data ss:Type="String">Serum MicroRNA-Based Risk Prediction for Stroke</Data></Cell>
    <Cell><Data ss:Type="String">MiR-1228-5p, miR-1268a, miR-1268b, miR-4433b-3p, miR-6090, miR-6752-5p, and miR-6803-5p could predict the risk of cerebrovascular disorder before the onset of stroke</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31136284</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-6090</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA profiling of peripheral blood enriched for circulating tumor cells (CTCs) in testicular germ cell tumors (TGCTs)</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA expression profiling of PB enriched for CTCs in TGCTs is feasible, and show great promise in identifying new therapeutic targets and gene expression signature associated with treatment resistance</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-6126</Data></Cell>
    <Cell><Data ss:Type="String">Ubiquitous Release Of Exosomal Tumor Suppressor miR-6126 from Ovarian Cancer Cells</Data></Cell>
    <Cell><Data ss:Type="String">MiR-6126 inhibition promoted oncogenic behavior by leading ovarian cancer cells to release more exosomes</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27742688</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-615-3p</Data></Cell>
    <Cell><Data ss:Type="String">miR-615-3p expression level in bone marrow is associated with tumor recurrence in hepatocellular carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">MiR-615-3p in DTCs may play an important role in postoperative HCC recurrence, which suggests that?miR-615-3p?is a potential target molecule for regulating postoperative HCC recurrence</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26137255</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-615-3p</Data></Cell>
    <Cell><Data ss:Type="String">Molecular Pathways: Clinical Applications and Future Direction of Insulin-like Growth Factor-1 Receptor Pathway Blockade</Data></Cell>
    <Cell><Data ss:Type="String">A negative correlation between miR-615-3p levels and IGF2 has been identified in NSCLC specimens, with IGF2/IGFR1 interaction acting as a mediator of metastasis in several types of tumors</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26429980</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-615-3p</Data></Cell>
    <Cell><Data ss:Type="String">Plasma exosomal miRNAs-based prognosis in metastatic kidney cancer</Data></Cell>
    <Cell><Data ss:Type="String">Kaplan-Meier analysis confirmed the significant OS association of three miRs; miR-let-7i-5p (P=0.018, HR=0.49, 95% CI=0.21-0.84), miR-26a-1-3p (P=0.025, HR=0.43, 95% CI=0.10-0.84) and miR-615-3p (P=0.0007, HR=0.36, 95% CI=0.11-0.54)</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28969022</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-615-3p</Data></Cell>
    <Cell><Data ss:Type="String">miR-615-3p promotes proliferation and migration and inhibits apoptosis through its potential target CELF2 in gastric cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-615-3p promotes gastric cancer proliferation and migration by suppressing CELF2 expression for the first time, providing clues for future clinical practices</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29501762</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-615-3p</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA 615-3p Inhibits the Tumor Growth and Metastasis of NSCLC via Inhibiting IGF2</Data></Cell>
    <Cell><Data ss:Type="String">MiR-615-3p played important roles in the regulation of NSCLC growth and metastasis by targeting IGF2</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29562959</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-615-3p</Data></Cell>
    <Cell><Data ss:Type="String">Identification of microRNA-615-3p as a novel tumor suppressor in non-small cell lung cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-615-3p functions as a tumor suppressor in NSCLC, and may be a novel potential molecular therapeutic target for patients with NSCLC;The results revealed that overexpressed miR-615-3p markedly inhibited cell proliferation and colony formation in the 3 NSCLC cell lines compared with the cells overexpressing the negative control sequence (NC). Additional investigation revealed that miR-615-3p overexpression significantly induced apoptosis and cell cycle arrest at the G1 phase in the A549, H1299 and H1650 cell lines compared with the cells overexpressing NC. Finally, ectopic expression of miR-615-3p was found to repress the cell migration and invasion of the 3 lung cancer cell lines</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="String">?28454411</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-6165</Data></Cell>
    <Cell><Data ss:Type="String">Experimental Verification of a Predicted Intronic MicroRNA in Human NGFR Gene with a Potential Pro-Apoptotic Function</Data></Cell>
    <Cell><Data ss:Type="String">Some of the previously attributed functions of NGFR could be explained indirectly by co-transcription of mir-6165 in the cells.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22558167</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-6165</Data></Cell>
    <Cell><Data ss:Type="String">Regulatory networks between neurotrophins and miRNAs in brain diseases and cancers</Data></Cell>
    <Cell><Data ss:Type="String">MiR-6165 functions on its target genes, including neural stem cell-derived dendrite regulator (DAGLA) and Polycistin-1 (PKD1), but not on any p75NTR downstream pathways</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25544363</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-638</Data></Cell>
    <Cell><Data ss:Type="String">miR-638 is a new biomarker for outcome prediction of non-small cell lung cancer patients receiving chemotherapy</Data></Cell>
    <Cell><Data ss:Type="String">That serum miR-638 levels are associated with the survival of NSCLC patients and may be considered a potential independent predictor for NSCLC prognosis</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25952770</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-638</Data></Cell>
    <Cell><Data ss:Type="String">MiR-146a and miR-638 in BRCA1-deficient triple negative breast cancer tumors, as potential biomarkers for improved overall survival</Data></Cell>
    <Cell><Data ss:Type="String">MiR-146a and miR-638 are potential biomarkers for improved overall survival in patients with BRCA1-deficient TNBC tumors</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26835710</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-638</Data></Cell>
    <Cell><Data ss:Type="String">MiRNA-638 promotes autophagy and malignant phenotypes of cancer cells via directly suppressing DACT3</Data></Cell>
    <Cell><Data ss:Type="String">Our data in clinical tissue samples highlight miR-638 and?DACT3?as histological marker for cancer detection and their potentially therapeutic implications</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28108314</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-638</Data></Cell>
    <Cell><Data ss:Type="String">MiR-638 inhibits cervical cancer metastasis through Wnt/β-catenin signaling pathway and correlates with prognosis of cervical cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">MiR-638 might serve as a tumor suppressor. In the future, miR-638 might be regarded as a therapeutic target and a potential prognostic factor in human CC</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29271990</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-638</Data></Cell>
    <Cell><Data ss:Type="String">MiR-638 inhibits cervical cancer metastasis through Wnt/β-catenin signaling pathway and correlates with prognosis of cervical cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">In vitro assay showed that miR-638 overexpression suppressed cell migration and invasion of HeLa cells. The results of Western blot indicated that over-expression of miR-638 inhibited the activation of Wnt/β-catenin signaling pathway.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29271990</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-638</Data></Cell>
    <Cell><Data ss:Type="String">MiR-638 acts as a tumor suppressor gene in gastric cancer</Data></Cell>
    <Cell><Data ss:Type="String">In the cell lines, aberrant expression of miR-638 was related to the cell proliferation, cell cycle and invasion. We also found that SOX2 had a negative correlation with miR-638 in GC tissues, and miR-638 overexpression could decrease SOX2 expression level by directly binding the 3'-UTR of SOX2.in vitro, down-regulating SOX2 by siRNA could counteract the effect of miR-638 inhibitor on GC cells proliferation and invasion</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29296232</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-638</Data></Cell>
    <Cell><Data ss:Type="String">Downregulation of miR-638 promotes progression of breast cancer and is associated with prognosis of breast cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">The miR-638 could be considered as an independent prognostic factor for the patients (HR =0.321, 95% CI =0.117-0.882, P=0.027)</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30349320</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-638</Data></Cell>
    <Cell><Data ss:Type="String">Downregulation of miR-638 promotes progression of breast cancer and is associated with prognosis of breast cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">Downregulation of miR-638 was capable of promoting cell proliferation, migration, and invasion in MDA-MB-231 and MCF-7 cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30349320</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-638</Data></Cell>
    <Cell><Data ss:Type="String">miR-638 represses the stem cell characteristics of breast cancer cells by targeting E2F2</Data></Cell>
    <Cell><Data ss:Type="String">MiR-638 represses the characteristics and behaviors of BCSCs by targeting E2F2. MiR-638 may be a potential target for breast cancer therapy</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31410735</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-638</Data></Cell>
    <Cell><Data ss:Type="String">Exosomes released from pancreatic cancer cells are heterogeneous particle populations</Data></Cell>
    <Cell><Data ss:Type="String">Exosomes form heterogeneous particle populations and nSMase2 may be involved in the exosomal uptake of miR-638</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-639</Data></Cell>
    <Cell><Data ss:Type="String">miR-639 promotes the proliferation and invasion of breast cancer cell in vitro</Data></Cell>
    <Cell><Data ss:Type="String">A key role of miR-639 in breast cancer metastasis and support biological and clinical links between miR-639 and breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24917697</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-639</Data></Cell>
    <Cell><Data ss:Type="String">miR-639 is differentially expressed in NPC tissues of varying cancer stages, and suggests that quantifying circulating miR-639 may be of importance for non-invasive diagnosis and prognostic evaluation, and may have potential therapeutic utility</Data></Cell>
    <Cell><Data ss:Type="String">MiR-639 upregulation was associated with development of TC, miR-639 promoted cell proliferation and cell cycle by targeting CDKN1A in TC.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27829546</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-639</Data></Cell>
    <Cell><Data ss:Type="String">miR-639 is associated with advanced cancer stages and promotes proliferation and migration of nasopharyngeal carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">MiR-639 is differentially expressed in NPC tissues of varying cancer stages, and suggests that quantifying circulating miR-639 may be of importance for non-invasive diagnosis and prognostic evaluation, and may have potential therapeutic utility</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="String">?30546422</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-639</Data></Cell>
    <Cell><Data ss:Type="String">MiR-10b, miR-133a, miR-155 and miR-639 as non-invasive potential biomarkers in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-10b, miR-133a, miR-155 and miR-639 have a significant signature in the pathogenesis of breast cancer and can be used as non-invasive molecular biomarkers for breast cancer detection.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-664b-5p</Data></Cell>
    <Cell><Data ss:Type="String">PARP inhibitor increases chemosensitivity by upregulating miR-664b-5p in BRCA1-mutated triple-negative breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-664b-5p functions as a tumour suppressor and has an important role in the regulation of PARP inhibitors to increase chemosensitivity by targeting CCNE2</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28176879</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-6727-5p</Data></Cell>
    <Cell><Data ss:Type="String">Influence of hsa-miR-6727-5p on the proliferation, apoptosis, invasion and migration of Caski, Hela and SiHa cervical cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-6727-5p promoted the proliferation, invasion and migration of cervical cancer cells and inhibited the apoptosis through the overexpression or inhibition of hsa-miR-6727-5p</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28952216</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-6727-5p</Data></Cell>
    <Cell><Data ss:Type="String">High-throughput sequencing of circRNAs reveals novel insights into mechanisms of nigericin in pancreatic cancer</Data></Cell>
    <Cell><Data ss:Type="String">For example, the up-regulated circRNA_06429 had the potential biding sites of miR-1307-3p, miR-5002-3p, miR-6727-5p and miR-744-5p simultaneously</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31533620</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-6734-5p</Data></Cell>
    <Cell><Data ss:Type="String">miR-6734 Up-Regulates p21 Gene Expression and Induces Cell Cycle Arrest and Apoptosis in Colon Cancer Cells</Data></Cell>
    <Cell><Data ss:Type="String">MiR-6734 inhibits the growth of colon cancer cells by up-regulating p21 gene expression and subsequent induction of cell cycle arrest and apoptosis, suggesting its role as an important endogenous regulator of cancer cell proliferation and survival</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27509128</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-6738-5p</Data></Cell>
    <Cell><Data ss:Type="String">Altered Fecal Small RNA Profiles in Colorectal Cancer Reflect Gut Microbiome Composition in Stool Samples</Data></Cell>
    <Cell><Data ss:Type="String">The hsa-miR-200b-3p expression levels progressively increased whereas those of hsa-miR-6738-5p gradually decreased going from the healthy to the adenoma to the CRC group</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31530647</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-6778-5p</Data></Cell>
    <Cell><Data ss:Type="String">CircRNA CBL.11 suppresses cell proliferation by sponging miR-6778-5p in colorectal?cancer</Data></Cell>
    <Cell><Data ss:Type="String">CircRNA CBL.11 was increased in CRC cells and could function as a competing endogenous RNA (ceRNA) to regulate YWHAE expression by sponging miR-6778-5p, resulting in regulation the proliferation of CRC cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31438886</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-6797-5p</Data></Cell>
    <Cell><Data ss:Type="String">Parathyroid hormone-stimulation of Runx2 during osteoblast differentiation via the regulation of lnc-SUPT3H-1:16 (RUNX2-AS1:32) and miR-6797-5p</Data></Cell>
    <Cell><Data ss:Type="String">MiR-6797-5p controls osteoblast differentiation by targeting Runx2 expression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30562548</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-6805-5p</Data></Cell>
    <Cell><Data ss:Type="String">Progesterone receptor A promotes invasiveness and metastasis of luminal breast cancer by suppressing regulation of critical microRNAs by estrogen</Data></Cell>
    <Cell><Data ss:Type="String">MiR-6805-5p, miR-584-5p, miR-1228-5p, miR-501-5p, and miR-668-5p were also strongly up-regulated in other PR-A-Positive cell lines, including parental T47D cells, BT474 cells, and ZR-75-1 cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29162724</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-6875-5p</Data></Cell>
    <Cell><Data ss:Type="String">Novel combination of serum microRNA for detecting breast cancer in the early stage</Data></Cell>
    <Cell><Data ss:Type="String">MiRNA expressions were compared between patients with breast cancer and non-Breast cancer, and a combination of five miRNA (miR-246, miR-307-p, miR-634, miR-861-p and miR-875-p) was found to be able to detect breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26749252</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-6875-5p</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-6826 and 6875 in plasma are valuable non-invasive biomarkers that predict the efficacy of vaccine treatment against metastatic colorectal cancer</Data></Cell>
    <Cell><Data ss:Type="String">Although further clarification is needed regarding the functions of miR-6826 and miR-6875 and their relationship to immune-related molecules, plasma miR-6826 and miR-6875 may be useful negative biomarkers for predicting the efficacy of vaccine treatment</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27878288</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-6875-5p</Data></Cell>
    <Cell><Data ss:Type="String">Usefulness of serum microRNA as a predictive marker of recurrence and prognosis in biliary tract cancer after radical surgery</Data></Cell>
    <Cell><Data ss:Type="String">Using microarray analysis, we successfully identified six specific miRNAs (miR-1225-3p, miR-1234-3p, miR1260b, miR-1470, miR-6834-3p, and miR-6875-5p) associated with recurrence and prognosis of BTC after radical surgery</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30976046</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-6882-3p</Data></Cell>
    <Cell><Data ss:Type="String">Circular RNA Expression Profile and Analysis of Their Potential Function in Psoriasis</Data></Cell>
    <Cell><Data ss:Type="String">The top five MREs of hsa_circ_0061012 were hsa-miR-7157-5p, hsa-miR-4769-3p, hsa-miR-6817-5p, hsa-miR-4310, and hsa-miR-6882-3</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30278433</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-720</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNAs are exported from malignant cells in customized particles</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-720 is characterized by excessive release from breast cancer cells while retaining relatively low concentrations of miRNA in the cells and could be used to detect the presence of malignant cells in the body</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">22772984</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-720</Data></Cell>
    <Cell><Data ss:Type="String">miR-720 inhibits tumor invasion and migration in breast cancer by targeting TWIST1</Data></Cell>
    <Cell><Data ss:Type="String">MiR-720 inhibits tumor invasion and migration in breast cancer by targeting TWIST1</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24085799</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-720</Data></Cell>
    <Cell><Data ss:Type="String">miR-720 inhibits tumor invasion and migration in breast cancer by targeting TWIST1</Data></Cell>
    <Cell><Data ss:Type="String">MiR-720 is frequently decreased in breast cancer and manifests antimetastatic activity by downregulating TWIST1, presenting a novel mechanism of miRNA-mediated regulation of tumor metastasis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24085799</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-720</Data></Cell>
    <Cell><Data ss:Type="String">miR-720 is a downstream target of an ADAM8-induced ERK signaling cascade that promotes the migratory and invasive phenotype of triple-negative breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-720 promise as a biomarker for early detection of or treatment response of ADAM8-positive TNBC</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27039296</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-720</Data></Cell>
    <Cell><Data ss:Type="String">miR-720 is a downstream target of an ADAM8-induced ERK signaling cascade that promotes the migratory and invasive phenotype of triple-negative breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">MiR-720 is elevated in serum of patients with ADAM8-high TNBC and, in a group with other miRNAs downstream of ADAM8</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27039296</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-7-2-3p</Data></Cell>
    <Cell><Data ss:Type="String">A two miRNA classifier differentiates follicular thyroid carcinomas from follicular thyroid adenomas</Data></Cell>
    <Cell><Data ss:Type="String">The identified two-miR-classifier combining miR-486-5p and miR-7-2-3p had the accuracy of 62%, sensitivity of 82.1%, and specificity of 48.8%</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25258301</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-7-2-3p</Data></Cell>
    <Cell><Data ss:Type="String">Integrative microRNA-mRNA and protein-protein interaction analysis in pancreatic neuroendocrine tumors</Data></Cell>
    <Cell><Data ss:Type="String">In the miRNA-target gene regulatory network, hsa-miR-7-2-3p demonstrated the highest connectivities whereas KLF12 was the mRNAs with the highest connectivities. It suggested that hsamiR-7-2-3p and KLF12 may affect the tumorigenesis of pancreatic cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27424984</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-760</Data></Cell>
    <Cell><Data ss:Type="String">miRNA expression patterns in chemoresistant breast cancer tissues</Data></Cell>
    <Cell><Data ss:Type="String">MiR-760 might be biomarkers for the prognosis of breast cancer chemoresistance</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25451164</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-760</Data></Cell>
    <Cell><Data ss:Type="String">miR-760 mediates chemoresistance through inhibition of epithelial mesenchymal transition in breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">MiR-760 modulated chemoresistance through the epithelial-mesenchymal transition in breast cancer cells, providing a potential therapeutic target for treatment of drug-resistant breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27981531</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-760</Data></Cell>
    <Cell><Data ss:Type="String">The expression profiling of serum miR-92a, miR-375, and miR-760 in colorectal cancer: An Egyptian study</Data></Cell>
    <Cell><Data ss:Type="String">Serum level of miR-92a, miR-375, and miR-760 may serve as biomarkers of colorectal cancer in Egyptian patients with high diagnostic power for miR-760 and high prognostic power for miR-92a</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28618945</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-760</Data></Cell>
    <Cell><Data ss:Type="String">MiR-760 suppresses human colorectal cancer growth by targeting BATF3/AP-1/cyclinD1 signaling</Data></Cell>
    <Cell><Data ss:Type="String">MiR-760 inhibited CRC growth by downregulating BATF3/AP-1/ cyclinD1 signaling</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29661228</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-760</Data></Cell>
    <Cell><Data ss:Type="String">MiR-760 enhances TRAIL sensitivity in non-small cell lung cancer via targeting the protein FOXA1</Data></Cell>
    <Cell><Data ss:Type="String">MiR-760 should be considered as a tumor suppressor since it negatively regulates the oncogene protein FOXA1 and regulated TRAIL sensitivity in NSCLC cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29665655</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-7704</Data></Cell>
    <Cell><Data ss:Type="String">Human adipose mesenchymal stem cell-derived exosomal-miRNAs are critical factors for inducing antiproliferation signalling to A2780 and SKOV-3 ovarian cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">Several other miRNAs which belong to top 20 known exosomal miRNAs, have not been extensively investigated for their oncogene regulatory properties; these miRNAs include hsa-miR-7704, hsa-miR-6087, hsa-miR-22-3p, hsa-miR-4466, hsa-miR-4532, hsa-miR-7641, hsa-miR-4448, hsa-miR-3960, and hsa-miR-3687</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27929108</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-7704</Data></Cell>
    <Cell><Data ss:Type="String">Infection of Epstein-barr Virus in Type III Latency Modulates Biogenesis of Exosomes and the Expression Profile of Exosomal miRNAs in the Burkitt Lymphoma Mutu Cell Lines</Data></Cell>
    <Cell><Data ss:Type="String">MiR-7704 is upregulated in macrophages treated with a combination of interleukin-27 (IL-27) and macrophage colony stimulating factor.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30029522</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-7704</Data></Cell>
    <Cell><Data ss:Type="String">Small RNA sequences derived from pre-microRNAs in the supraspliceosome?</Data></Cell>
    <Cell><Data ss:Type="String">Nuclear miR-7704 negatively regulates the expression of the lincRNA HAGLR</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30203035</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-8064</Data></Cell>
    <Cell><Data ss:Type="String">OCT4B1 Promoted EMT and Regulated the Self-renewal of Cancer Stem Cells (CSCs) in Colorectal Cancer: Effects Associated with the Balance of miR-8064/PLK1</Data></Cell>
    <Cell><Data ss:Type="String">OCT4B1 may be involved in regulating the self-renewal of colorectal CSCs through EMT, which is at least partially due to the miR-8064/PLK1 balance. This study indicates that OCT4B1 is a potential therapeutic target for CRC by targeting CSCs</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-8078</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA Expression Profile on Solid Subtype of Invasive Lung Adenocarcinoma Reveals a Panel of Four miRNAs to Be Associated with Poor Prognosis in Chinese Patients</Data></Cell>
    <Cell><Data ss:Type="String">There are also novel, differentially expressed miRNAs that had never before been identified as differentially expressed associated in malignancy, including miR-629.5p, miR-4428, miR-4647, and miR-8078</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27698898</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-93-5p</Data></Cell>
    <Cell><Data ss:Type="String">Differential expression of exosomal miRNAs between breast cancer patients with and without recurrence</Data></Cell>
    <Cell><Data ss:Type="String">Of 384 miRNAs, three miRNAs (miR-338-3p, miR-340-5p, and miR-124-3p) were significantly upregulated and eight (miR-29b-3p, miR-20b-5p, miR-17-5p, miR-130a-3p, miR-18a-5p, miR-195-5p, miR-486-5p, and miR-93-5p) were significantly downregulated in the patients with recurrence</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29050253</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-93-5p</Data></Cell>
    <Cell><Data ss:Type="String">miR-93 inhibits the invasive potential of triple-negative breast cancer cells in vitro via protein kinase WNK1</Data></Cell>
    <Cell><Data ss:Type="String">Further in vivo studies are required to ascertain the miR-93-WNK1-metastasis cascade, that has potential implications in breast cancer therapy</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27840899</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-93-5p</Data></Cell>
    <Cell><Data ss:Type="String">MiR-93-5p inhibits the EMT of breast cancer cells via targeting MKL-1 and STAT3</Data></Cell>
    <Cell><Data ss:Type="String">MiR-93-5p regulates MKL-1 and STAT3 to affect EMT controlling breast cancer cell migration</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28499590</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-93-5p</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-93 promotes proliferation and metastasis of gastric cancer via targeting TIMP2</Data></Cell>
    <Cell><Data ss:Type="String">MiR-93 might be a promising biomarker and therapeutic target for treatment of gastric cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29220395</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-93-5p</Data></Cell>
    <Cell><Data ss:Type="String">MicroRNA-93 promotes proliferation and metastasis of gastric cancer via targeting TIMP2</Data></Cell>
    <Cell><Data ss:Type="String">MiR-93 serves as a tumor promoter in human gastric carcinogenesis by targeting TIMP2</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29220395</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-93-5p</Data></Cell>
    <Cell><Data ss:Type="String">miR-93-5p Transferred by Exosomes Promotes the Proliferation of Esophageal Cancer Cells?via?Intercellular Communication by Targeting PTEN</Data></Cell>
    <Cell><Data ss:Type="String">Upregulation of plasma miR-93-5p expression significantly increases the risk of esophageal cancer and is associated with poor prognosis</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29673440</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-93-5p</Data></Cell>
    <Cell><Data ss:Type="String">miR-93-5p Transferred by Exosomes Promotes the Proliferation of Esophageal Cancer Cells?via?Intercellular Communication by Targeting PTEN</Data></Cell>
    <Cell><Data ss:Type="String">MiR-93-5p transferred by exosomes promotes the proliferation of recipient esophageal cancer cells and affects the expression of PTEN and its downstream proteins p21 and cyclin D1</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29673440</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-93-5p</Data></Cell>
    <Cell><Data ss:Type="String">miR-93-5p enhance lacrimal gland adenoid cystic carcinoma cell tumorigenesis by targeting BRMS1L.</Data></Cell>
    <Cell><Data ss:Type="String">MiR-93 promotes LACC cell migration, invasion, and proliferation via targeting downregulation of BRMS1L through regulation of Wnt signaling pathway</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29760585</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-937-5p</Data></Cell>
    <Cell><Data ss:Type="String">miRNA expression patterns in normal breast tissue and invasive breast cancers of BRCA1 and BRCA2 germ-line mutation carriers</Data></Cell>
    <Cell><Data ss:Type="String">MiR-3676-5p and miR-937-5p (up-regulated in BRCA1/2- associated breast carcinomas and not deregulated in sporadic breast carcinomas)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26378051</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-937-5p</Data></Cell>
    <Cell><Data ss:Type="String">miR-30a-5p enhances paclitaxel sensitivity in non-small cell lung cancer through targeting BCL-2 expression</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-937-5p was downregulated in our RTHF-treated A549 cells, and it has been observed to be highly expressed in paclitaxel-resistant A549 cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28487996</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-939</Data></Cell>
    <Cell><Data ss:Type="String">Breast cancer-secreted hsa-miR-939 downregulates VE-cadherin and destroys the barrier function of endothelial monolayers</Data></Cell>
    <Cell><Data ss:Type="String">Hsa-miR-939 downregulates VE-cadherin and destroys the barrier function of endothelial monolayers and an extracellular tumorigenic effect</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">27693459</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-939</Data></Cell>
    <Cell><Data ss:Type="String">Circulating microRNAs, miR-939, miR-595, miR-519d and miR-494, Identify Cirrhotic Patients with HCC</Data></Cell>
    <Cell><Data ss:Type="String">In the validation set, miR-939, miR-595 and miR-519d were shown to differentiate cirrhotic patients with and without HCC. MiR-939 and miR-595 are independent factors for HCC. ROC curves of miR-939, miR-595 and miR-519d displayed that AUC was higher than AFP</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26509672</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">hsa-miR-939</Data></Cell>
    <Cell><Data ss:Type="String">Prognostic value of 5-microRNA based signature in T2-T3N0 colon cancer</Data></Cell>
    <Cell><Data ss:Type="String">Low expression of miR-1300 and miR-939 was significantly correlated with shorter distant metastasis-free survival (DMFS) in Cox univariate analysis (p.adjusted?=?0.049)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27485175</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HTR7</Data></Cell>
    <Cell><Data ss:Type="String">Exosomes enriched in stemness/metastatic-related mRNAS promote oncogenic potential in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Stemness markers and enhance proliferation,migration and invasion abilities of neighboring cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">26528758</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HTR7</Data></Cell>
    <Cell><Data ss:Type="String">Expressed pseudogenes in the transcriptional landscape of human cancers</Data></Cell>
    <Cell><Data ss:Type="String">Parent genes HTR7, CNN2, MSN, and TAGLN2 are DE; they generate pseudogenes, which are specifically expressed in prostate cancer samples</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22726445</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">HTR7</Data></Cell>
    <Cell><Data ss:Type="String">Breast Cancer Gene Expression Profile in Post-Menopausal Patients Supplemented with Vitamin D</Data></Cell>
    <Cell><Data ss:Type="String">Differentially expressed genes were involved in the regulation of cell cycle (SMAD2, cyclin E, YWHAQ , 14-3-3 family ) and calcium signalling (HTR7, PTGER1?and?PTGER2)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">IGF1R</Data></Cell>
    <Cell><Data ss:Type="String">Proteomic Profiling of Exosomes Secreted by Breast Cancer Cells with Varying Metastatic Potential</Data></Cell>
    <Cell><Data ss:Type="String">Presumably aid in targeting the primary cancer cells to specific metastatic sites</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29115712</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">IGF1R</Data></Cell>
    <Cell><Data ss:Type="String">Prognostic significance of insulin growth factor-I receptor and insulin growth factor binding protein-3 expression in primary breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">IGF-IR expression in primary breast cancer is an independent favorable prognostic factor.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">20204283</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">IGF1R</Data></Cell>
    <Cell><Data ss:Type="String">Insulin-like growth factor receptor (IGF-1R) in breast cancer subtypes</Data></Cell>
    <Cell><Data ss:Type="String">IGF-1R correlates with good prognostic markers among patients with early breast cancer and is differentially expressed with variable prognostic impact among breast cancer subtypes.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21574055</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">IGF1R</Data></Cell>
    <Cell><Data ss:Type="String">The impact of IGF-1R expression on the outcomes of patients with breast cancer: a meta-analysis</Data></Cell>
    <Cell><Data ss:Type="String">IGF-1R expression has different prognostic values for patients with breast cancers of different molecular subtypes. It was a favorable prognostic indicator in unselected breast cancers and hormone-receptor-positive cancers, but indicated poor survival in triple-negative breast cancers</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25674003</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">IGF1R</Data></Cell>
    <Cell><Data ss:Type="String">Role of IGF1R in Breast Cancer Subtypes, Stemness, and Lineage Differentiation</Data></Cell>
    <Cell><Data ss:Type="String">The reduction in mammary gland morphogenesis observed upon loss of IGF1/IGF1R signaling is a result of decreased cell cycle progression and increased apoptosis</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25964777</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">IL1RAP</Data></Cell>
    <Cell><Data ss:Type="String">Proteomic Profiling of Exosomes Secreted by Breast Cancer Cells with Varying Metastatic Potential</Data></Cell>
    <Cell><Data ss:Type="String">Presumably aid in targeting the primary cancer cells to specific metastatic sites</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29115712</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">IL1RAP</Data></Cell>
    <Cell><Data ss:Type="String">Selective killing of candidate AML stem cells by antibody targeting of IL1RAP</Data></Cell>
    <Cell><Data ss:Type="String">IL1RAP is a promising new therapeutic target in AML</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23479569</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">IL1RAP</Data></Cell>
    <Cell><Data ss:Type="String">Antibodies targeting human IL1RAP (IL1R3) show therapeutic effects in xenograft models of acute myeloid leukemia</Data></Cell>
    <Cell><Data ss:Type="String">Collectively, these results provide important evidence in support of IL1RAP as a target for antibody-based treatment of AML</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26261316</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">IL1RAP</Data></Cell>
    <Cell><Data ss:Type="String">Antibodies targeting human IL1RAP (IL1R3) show therapeutic effects in xenograft models of acute myeloid leukemia</Data></Cell>
    <Cell><Data ss:Type="String">Critical evidence in support of a rapid clinical development of an antibody-based anti-IL1RAP therapy in AML</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26261316</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">IL1RAP</Data></Cell>
    <Cell><Data ss:Type="String">SRSF10-mediated IL1RAP alternative splicing regulates cervical cancer oncogenesis via mIL1RAP-NF-κB-CD47 axis</Data></Cell>
    <Cell><Data ss:Type="String">SRSF10-mIL1RAP-CD47 axis could be an attractive therapeutic target for the treatment of cervical cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29429992</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">IL1RAP</Data></Cell>
    <Cell><Data ss:Type="String">IL1RAP potentiates multiple oncogenic signaling pathways in AML</Data></Cell>
    <Cell><Data ss:Type="String">Our study provides a new mechanistic basis for the efficacy of IL1RAP targeting in AML and reveals a novel role for this protein in the pathogenesis of the disease</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29773641</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ITGB1</Data></Cell>
    <Cell><Data ss:Type="String">Proteomic Profiling of Exosomes Secreted by Breast Cancer Cells with Varying Metastatic Potential</Data></Cell>
    <Cell><Data ss:Type="String">Presumably aid in targeting the primary cancer cells to specific metastatic sites</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29115712</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ITGB1</Data></Cell>
    <Cell><Data ss:Type="String">β1 integrin inhibitory antibody induces apoptosis of breast cancer cells, inhibits growth and distinguishes malignant from normal phenotype in three dimensional cultures and in vivo</Data></Cell>
    <Cell><Data ss:Type="String">Beta(1) integrin is a promising therapeutic target, and that the three-dimensional lrECM culture assay can be used to effectively distinguish malignant and normal tissue response to therapy</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">16452209</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ITGB1</Data></Cell>
    <Cell><Data ss:Type="String">β1 integrin inhibitory antibody induces apoptosis of breast cancer cells, inhibits growth and distinguishes malignant from normal phenotype in three dimensional cultures and in vivo</Data></Cell>
    <Cell><Data ss:Type="String">ITGB1 inhibition resulted in a significant loss of cancer cells, associated with a decrease in proliferation and increase in apoptosis, and a global change in the composition of residual colonies</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">16452209</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ITGB1</Data></Cell>
    <Cell><Data ss:Type="String">Gene expression profiling combined with functional analysis identify integrin beta1 (ITGB1) as a potential prognosis biomarker in triple negative breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Gene expression profiling combined with functional analysis identify integrin beta1 (ITGB1) as a  potential candidate biomarker for breast cancer cells migration, invasion and TNBC patients-survival in triple negative?breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26675717</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ITGB1</Data></Cell>
    <Cell><Data ss:Type="String">Gene expression profiling combined with functional analysis identify integrin beta1 (ITGB1) as a potential prognosis biomarker in triple negative breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Silencing of ITGB1 inhibited TNBC cell migration, invasion and store-operated calcium influx</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26675717</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ITGB1</Data></Cell>
    <Cell><Data ss:Type="String">β1 Integrin is essential for fascin-mediated breast cancer stem cell function and disease progression</Data></Cell>
    <Cell><Data ss:Type="String">There was a significant relationship between fascin and ITGB1 co-expression and short disease-free as well as overall survival in chemo-treated breast cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30719702</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ITGB1</Data></Cell>
    <Cell><Data ss:Type="String">β1 Integrin is essential for fascin-mediated breast cancer stem cell function and disease progression</Data></Cell>
    <Cell><Data ss:Type="String">Fascin-mediated regulation of ITGB1 was critical for several breast cancer cell functions including adhesion to different extracellular matrix, self-renewability and chemoresistance.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30719702</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ITGB1</Data></Cell>
    <Cell><Data ss:Type="String">Tenascin C interacts with integrin receptors to promote breast cancer metastasis to the lungs</Data></Cell>
    <Cell><Data ss:Type="String">Two integrin receptors of the mammary gland (ITGB1 and ITGB3) as the receptors mediating the TNC pro-metastatic signaling in triple-negative breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ITGB7</Data></Cell>
    <Cell><Data ss:Type="String">Integrin β7-mediated regulation of multiple myeloma cell adhesion, migration, and invasion</Data></Cell>
    <Cell><Data ss:Type="String">Our findings support a role for integrin-β7 in MM-cell adhesion, migration, and BM homing, and pave the way for a novel therapeutic approach targeting this molecule.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21474670</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ITGB7</Data></Cell>
    <Cell><Data ss:Type="String">Integrin β7-mediated regulation of multiple myeloma cell adhesion, migration, and invasion</Data></Cell>
    <Cell><Data ss:Type="String">ITGB7 knockdown inhibited focal adhesion kinase (FAK) and Src phosphorylation, Rac1 activation, and SUMOylation, reduced VEGF production in MM-BM stem cell cocultures and attenuated p65-NF-κB activity.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21474670</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">ITGB7</Data></Cell>
    <Cell><Data ss:Type="String">β7 integrins contribute to intestinal tumor growth in mice.</Data></Cell>
    <Cell><Data ss:Type="String">Using chemically induced and spontaneous intestinal tumor models we showed that lack of β7 integrin significantly impairs tumor growth without affecting tumor frequencies, with a mild translatable effect on overall survival. </Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30235302</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">IVL</Data></Cell>
    <Cell><Data ss:Type="String">Keratoacanthoma and squamous cell carcinoma of the skin: Immunohistochemical localization of involucrin and keratin proteins</Data></Cell>
    <Cell><Data ss:Type="String">Involucrin may serve as a diagnostic aid in differentiating between squamous cell carcinomas and keratoacanthoma</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">2419374</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">IVL</Data></Cell>
    <Cell><Data ss:Type="String">Squamoid features and expression of involucrin in primary breast carcinoma associated with high histological grade, tumour cell necrosis and recurrence sites</Data></Cell>
    <Cell><Data ss:Type="String">Involucrin, a marker of terminal keratinocyte differentiation, was expressed in a subset of tumours</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">9166948</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">IVL</Data></Cell>
    <Cell><Data ss:Type="String">Brk expression may affect the differentiation status of breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">Brk and involucrin may be coregulated and that inducers of differentiation such as vitamin D3 could be considered potential therapeutic strategies</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">3300779</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">KISS1R</Data></Cell>
    <Cell><Data ss:Type="String">Exosomes enriched in stemness/metastatic-related mRNAS promote oncogenic potential in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Stemness markers and enhance proliferation,migration and invasion abilities of neighboring cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">26528758</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">KISS1R</Data></Cell>
    <Cell><Data ss:Type="String">GPR54 (KISS1R) Transactivates EGFR to Promote Breast Cancer Cell Invasiveness</Data></Cell>
    <Cell><Data ss:Type="String">The stability of the receptor complex formation was increased upon treatment of cells by Kp-10. Taken together, our findings suggest a novel mechanism by which Kp signaling via GPR54 stimulates breast cancer cell invasiveness</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21738726</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">KISS1R</Data></Cell>
    <Cell><Data ss:Type="String">Haploinsufficiency in the prometastasis Kiss1 receptor Gpr54 delays breast tumor initiation, progression, and lung metastasis</Data></Cell>
    <Cell><Data ss:Type="String">Kiss1r attenuation was sufficient to delay breast tumor initiation, progression, and metastasis through inhibitory effects on the downstream G伪q-p63RhoGEF-RhoA signaling pathway</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21852382</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">KISS1R</Data></Cell>
    <Cell><Data ss:Type="String">KISS1R Induces Invasiveness of Estrogen Receptor-Negative Human Mammary Epithelial and Breast Cancer Cells</Data></Cell>
    <Cell><Data ss:Type="String">The ERα status of mammary cells dictates whether KISS1R may be a novel clinical target for treating breast cancer metastasis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23525242</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">KISS1R</Data></Cell>
    <Cell><Data ss:Type="String">Kisspeptin/KISS1R System in Breast Cancer</Data></Cell>
    <Cell><Data ss:Type="String">KP/KISS1R pathway plays detrimental roles in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24155777</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">KISS1R</Data></Cell>
    <Cell><Data ss:Type="String">KISS1R signaling promotes invadopodia formation in human breast cancer cell via β-arrestin2/ERK</Data></Cell>
    <Cell><Data ss:Type="String">Targeting the KISS1R signaling axis might be a promising strategy to inhibit invasiveness and metastasis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26721186</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">KISS1R</Data></Cell>
    <Cell><Data ss:Type="String">G protein-coupled KISS1 receptor is overexpressed in triple negative breast cancer and promotes drug resistance</Data></Cell>
    <Cell><Data ss:Type="String">KISS1R represents a potentially novel therapeutic target to restore drug sensitivity in TNBC patients</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28422142</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">KRT14</Data></Cell>
    <Cell><Data ss:Type="String">Proteomic Profiling of Exosomes Secreted by Breast Cancer Cells with Varying Metastatic Potential</Data></Cell>
    <Cell><Data ss:Type="String">Presumably aid in targeting the primary cancer cells to specific metastatic sites</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29115712</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">KRT14</Data></Cell>
    <Cell><Data ss:Type="String">Collective invasion in breast cancer requires a conserved basal epithelial program</Data></Cell>
    <Cell><Data ss:Type="String">Similarly, KRT14-expressing breast cancer cells are only capable of leading invasion through a stromal ECM that is rich in fibrillar collagen and deficient in collagen IV?</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24332913</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">KRT14</Data></Cell>
    <Cell><Data ss:Type="String">Identification of Distinct Basal and Luminal Subtypes of Muscle-Invasive Bladder Cancer with Different Sensitivities to Frontline Chemotherapy</Data></Cell>
    <Cell><Data ss:Type="String">ΔNp63α knockdown in human bladder or breast cancer cells result in down regulated expression of basal biomarkers such as CD44, KRT5, KRT14, and CDH3</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24525232</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">KRT14</Data></Cell>
    <Cell><Data ss:Type="String">Polyclonal breast cancer metastases arise from collective dissemination of keratin 14-expressing tumor cell clusters</Data></Cell>
    <Cell><Data ss:Type="String">To dissect this list further, we next ranked genes by their association with Krt14 transcript levels [487 genes at a false-discovery rate (FDR) &lt; 0.05]. The top four genes most correlated with Krt14 transcript expression were enriched for multiple major metastasis effector genes that promote metastatic niche remodeling (Tnc, AdamTs1, Jag1) and metastasis survival</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26831077</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">KRT14</Data></Cell>
    <Cell><Data ss:Type="String">Foxa1 is essential for mammary duct formation</Data></Cell>
    <Cell><Data ss:Type="String">A potentially powerful model for complete ablation of Foxa1 in mammary epithelial cells using Krt14-driven Cre expression in an inducible manner, such as Krt14-rtTA;Tet-On-Cre</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26919034</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">KRT14</Data></Cell>
    <Cell><Data ss:Type="String">Normal Breast-Derived Epithelial Cells with Luminal and Intrinsic Subtype-Enriched Gene Expression Document Interindividual Differences in Their Differentiation Cascade</Data></Cell>
    <Cell><Data ss:Type="String">RNA-seq and PAM50-intrinsic subtype clustering identified these cell lines as the &quot;normal&quot; counterparts of luminal A, basal, and normal-like subtypes and validated via immunostaining with basal-enriched KRT14 and luminal-enriched KRT19</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29997232</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">LDHA</Data></Cell>
    <Cell><Data ss:Type="String">Proteomic Profiling of Exosomes Secreted by Breast Cancer Cells with Varying Metastatic Potential</Data></Cell>
    <Cell><Data ss:Type="String">Presumably aid in targeting the primary cancer cells to specific metastatic sites</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29115712</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">LDHA</Data></Cell>
    <Cell><Data ss:Type="String">Upregulation of lactate dehydrogenase A by ErbB2 through heat shock factor 1 promotes breast cancer cell glycolysis and growth</Data></Cell>
    <Cell><Data ss:Type="String">Overexpression of ErbB2 increased the expression of glycolysis-regulating molecules lactate dehydrogenase A (LDH-A) and heat shock factor 1 (HSF1). ErbB2 activated HSF1, indicated by the increased HSF1 trimer formation, and promoted HSF1 protein synthesis. HSF1 bound to LDH-A promoter and the downregulation of HSF1 reduced the expression of LDH-A and subsequently decreased cancer cell glycolysis and growth.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19668225</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">LDHA</Data></Cell>
    <Cell><Data ss:Type="String">High expressions of LDHA and AMPK as prognostic biomarkers for breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">LDHA and AMPK as promising prognostic biomarkers for breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27598996</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">LDHA</Data></Cell>
    <Cell><Data ss:Type="String">Tumor LDH-A expression and serum LDH status are two metabolic predictors for triple negative breast cancer brain metastasis</Data></Cell>
    <Cell><Data ss:Type="String">Tumor LDH-A expression, serum LDH status, and the slope of serum LDH status were closely associated with triple negative breast cancer brain metastasis and brain metastasis free survival.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28729678</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">LINC00536</Data></Cell>
    <Cell><Data ss:Type="String">Long non-coding RNAs as prognostic markers in human breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">LINC00536 may serve as prognostic markers for breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26942882</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">LINC00536</Data></Cell>
    <Cell><Data ss:Type="String">Identification of an lncRNA-miRNA-mRNA interaction mechanism in breast cancer based on bioinformatic analysis</Data></Cell>
    <Cell><Data ss:Type="String">The network of lncRNA miRNA mRNA interactions (LINC00536) will facilitate further experimental studies and may be used to refine biomarker predictions for developing novel therapeutic approaches in breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28849135</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">LINC00536</Data></Cell>
    <Cell><Data ss:Type="String">Systematic analysis of lncRNA-miRNA-mRNA competing endogenous RNA network identifies four-lncRNA signature as a prognostic biomarker for breast cancer</Data></Cell>
    <Cell><Data ss:Type="String"> 4 lncRNA biomarkers in the ceRNA network may be independent prognostic signatures in predicting the survival of breast cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30261893</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">LINC00536</Data></Cell>
    <Cell><Data ss:Type="String">High LINC00536 expression promotes tumor progression and poor prognosis in bladder cancer</Data></Cell>
    <Cell><Data ss:Type="String"> LINC00536 promoted BC progression by modulating the Wnt3a/β-Catenin signaling.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30851243</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">LINC00536</Data></Cell>
    <Cell><Data ss:Type="String">Identification of competitive endogenous RNAs network in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">The expression levels of LINC00536 (P = 8.1918e-4) and ADAMTS9-S1 (2.94e-3) were associated with poor overall suvival</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30932362</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">LINC00536</Data></Cell>
    <Cell><Data ss:Type="String">Comprehensive analysis of the aberrantly expressed lncRNA associated ceRNA network in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">LINC00536 and WT1-AS, were associated with overall survival</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31059025</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">LINC00578</Data></Cell>
    <Cell><Data ss:Type="String">LncRNAs are altered in lung squamous cell carcinoma and lung adenocarcinoma</Data></Cell>
    <Cell><Data ss:Type="String">LINC00578 act as oncogenes and lncRNA-regulating transcription factors provide novel targets for anti-lung cancer therapeutics</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27903974</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">LINC00578</Data></Cell>
    <Cell><Data ss:Type="String">Long non-coding RNA LINC00346,?LINC00578, LINC00673, LINC00671, LINC00261, and SNHG9 are novel prognostic markers for pancreatic cancer</Data></Cell>
    <Cell><Data ss:Type="String">LINC00578 was novel prognostic markers for pancreatic cancer</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30210701</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">LINC00578</Data></Cell>
    <Cell><Data ss:Type="String">Systematic identification of lincRNA-based prognostic biomarkers by integrating lincRNA expression and copy number variation in lung adenocarcinoma</Data></Cell>
    <Cell><Data ss:Type="String">Computational analysis entailing integration of expression and copy number alteration data revealed five prognostic lincRNAs: RBPMS-S1, TDRKH-S1, LINC00578, RP11-70 M17.2 and LINC00941</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30226269</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">LINC00578</Data></Cell>
    <Cell><Data ss:Type="String">Expression profiles of long noncoding RNAs in lung adenocarcinoma</Data></Cell>
    <Cell><Data ss:Type="String">LINC00578 was identified as a promising biomarker and therapeutic target for lung adenocarcinoma.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30233202</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">LINC00637</Data></Cell>
    <Cell><Data ss:Type="String">A combined epigenome- and transcriptome-wide association study of the oral masticatory mucosa assigns CYP1B1 a central role for epithelial health in smokers.</Data></Cell>
    <Cell><Data ss:Type="String">LINC00673 was significantly hypomethylated in smokers in our study at three individual CpGs, which was shown to be upregulated in tongue squamous cell carcinoma </Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31331382</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">LINC00658</Data></Cell>
    <Cell><Data ss:Type="String">Copy number variations of colorectal cancer by whole exome sequencing data</Data></Cell>
    <Cell><Data ss:Type="String">LINC00658 has copy number variations of colorectal cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">LINC00992</Data></Cell>
    <Cell><Data ss:Type="String">Identification and Validation of Long Noncoding RNA Biomarkers in human non-small-cell lung carcinomas</Data></Cell>
    <Cell><Data ss:Type="String">LINC00992 could be further exploited for the development of useful biomarkers in diagnosis, prognosis, and treatment of NSCLC.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25590602</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">LINC00992</Data></Cell>
    <Cell><Data ss:Type="String">Bronchial epithelial cells from cystic fibrosis patients express a specific long non-coding RNA signature upon Pseudomonas aeruginosa infection</Data></Cell>
    <Cell><Data ss:Type="String">LINC00992 has been shown to be expressed in lungs, kidneys and salivary glands </Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28611953</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">LINC00992</Data></Cell>
    <Cell><Data ss:Type="String">Systematic identification of non-coding pharmacogenomic landscape in cancer</Data></Cell>
    <Cell><Data ss:Type="String">LINC00992 in primary tumors increases along with the disease progression and correlates with poor patient survivals in multiple cancer types that are routinely treated with chemotherapy</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30093685</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">LINC01354</Data></Cell>
    <Cell><Data ss:Type="String">Comprehensive analysis of differential expression profiles of mRNAs and lncRNAs and identification of a 14-lncRNA prognostic signature for patients with colon adenocarcinoma</Data></Cell>
    <Cell><Data ss:Type="String">LINC01354 was mainly involved in vascular smooth muscle contraction and the cGMP-PKG signaling pathway</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29565464</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">LINC01354</Data></Cell>
    <Cell><Data ss:Type="String">Identification of differential expressed lnc RNA s in human thyroid cancer by a genome-wide analyses</Data></Cell>
    <Cell><Data ss:Type="String">The dysregulated lncRNAs genomic loci contains copy number amplification or deletion, such as LINC01354, LINC01341, LINC00595, and LINC01519, suggesting that genomic alterations might involve in part of these lncRNAs dysregulation in thyroid cancer.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29923329</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">LINC01354</Data></Cell>
    <Cell><Data ss:Type="String">A 15-lncRNA signature predicts survival and functions as a ceRNA in patients with colorectal cancer</Data></Cell>
    <Cell><Data ss:Type="String">LINC01354 expression signature was discovered as a prognostic indicator for patients with CRC, which may act as competing endogenous RNA (ceRNAs) to play a crucial role in the modulation of cancer-related pathways.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30510449</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">LINC01354</Data></Cell>
    <Cell><Data ss:Type="String">LINC01354 interacting with hnRNP-D contributes to the proliferation and metastasis in colorectal cancer through activating Wnt/β-catenin signaling pathway</Data></Cell>
    <Cell><Data ss:Type="String">Novel regulatory axis of LINC01354/hnRNP-D/Wnt/β-catenin might be in favor of exploring novel therapeutic regimens for the clinical treatment of colorectal cancer </Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30987669</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">LINC01354</Data></Cell>
    <Cell><Data ss:Type="String">Analysis of methylation-driven genes for predicting the prognosis of patients with head and neck squamous cell carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">LINC01354 could be used as independent prognostic markers and thus might be potential drug targets</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31264288</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MEF2A</Data></Cell>
    <Cell><Data ss:Type="String">The MEF2-HDAC axis controls proliferation of mammary epithelial cells and acini formation in vitro</Data></Cell>
    <Cell><Data ss:Type="String">In cells transformed by the oncogene HER2 (ERBB2), acini morphogenesis is altered, MEF2 transcription is repressed and HDAC7 is continuously expressed</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26403201</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MEF2A</Data></Cell>
    <Cell><Data ss:Type="String">The co-existence of transcriptional activator and transcriptional repressor MEF2 complexes influences tumor aggressiveness</Data></Cell>
    <Cell><Data ss:Type="String">In leiomyosarcomas (LMS), this two-faced trait of MEF2 is relevant for tumor aggressiveness</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28419090</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MEF2A</Data></Cell>
    <Cell><Data ss:Type="String">MEF2 signaling and human diseases</Data></Cell>
    <Cell><Data ss:Type="String">MEF2 family is closely associated with various signaling pathways, including Ca2+ signaling, MAP kinase signaling, Wnt signaling, PI3K/Akt signaling, etc. microRNAs also contribute to regulate the activities of MEF2</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29340119</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MEF2A</Data></Cell>
    <Cell><Data ss:Type="String">MEF2 plays a significant role in the tumor inhibitory mechanism of encapsulated RENCA cells via EGF receptor signaling in target tumor cells</Data></Cell>
    <Cell><Data ss:Type="String">Factors secreted by RENCA macrobeads significantly up-regulated the activity of the MEF2 transcription factor as well as altered the transcription of MEF2b and MEF2d isoforms in targeted tumor cells. Suppression of individual or multiple MEF2 isoforms in target tumor cells markedly reduced the growth inhibitory effects of RENCA macrobeads</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30514247</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MIR7-3HG</Data></Cell>
    <Cell><Data ss:Type="String">MIR7-HG, a MYC-dependent modulator of cell proliferation, inhibits autophagy by a regulatory loop involving AMBRA1</Data></Cell>
    <Cell><Data ss:Type="String">MIR7-3HG as an anti-autophagic MIRNA that may affect oncogenesis through the regulation of the tumor suppressor AMBRA1</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28059583</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MIR7-3HG</Data></Cell>
    <Cell><Data ss:Type="String">A 7-lncRNA signature predict prognosis of Uterine corpus endometrial carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">Our study revealed that the MIR7-3HG could be used to predict the prognosis of UCEC and for postoperative treatment and follow-up.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31168849</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MRPL15</Data></Cell>
    <Cell><Data ss:Type="String">Mitochondrial markers predict recurrence, metastasis and tamoxifen-resistance in breast cancer patients: Early detection of treatment failure with companion diagnostics</Data></Cell>
    <Cell><Data ss:Type="String">MRPL15 had the best prognostic value</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28978152</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MRPL21</Data></Cell>
    <Cell><Data ss:Type="String">The galanin signaling cascade is a candidate pathway regulating oncogenesis in human squamous cell carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">MRPL21 (rank 6), which is located near GAL in locus 11q13.2, has been suggested to play a role in carcinogenesis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">18973137</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MRPL21</Data></Cell>
    <Cell><Data ss:Type="String">Gene expression profiling: Canonical molecular changes and clinicopathological features in sporadic colorectal cancers</Data></Cell>
    <Cell><Data ss:Type="String">Amongst 47 differentially expressed genes, seven (PISD, NIBP, BAI2, STOML1, MRPL21, MRPL16, and MKKS) were newly found to correlate with tumorigenesis and tumor growth</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19034969</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MRPL21</Data></Cell>
    <Cell><Data ss:Type="String">Mitochondrial ribosomes in cancer</Data></Cell>
    <Cell><Data ss:Type="String">Among the proteins associated with these processes, mammalian mitochondrial ribosomal proteins (i.e. MRPL9, MRPL21, MRPL39) showed high correlation, which function in RNA synthesis and processing as well as protein synthesis and translation in cytosol and/or mitochondria and are necessary for the fast growth of tumor cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28445780</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MRPL4</Data></Cell>
    <Cell><Data ss:Type="String">An Integrating Approach for Genome-Wide Screening of MicroRNA Polymorphisms Mediated Drug Response Alterations</Data></Cell>
    <Cell><Data ss:Type="String"> a new discovery that an SNP (rs751012151) in MRPL4 can be downregulated by hsa-miR-6089 and decrease drug resistance in our database (?kcal/mol)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28480217</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MRPL4</Data></Cell>
    <Cell><Data ss:Type="String">Proteomic Profiling of Human Prostate Cancer-associated Fibroblasts (CAF) Reveals LOXL2-dependent Regulation of the Tumor Microenvironment</Data></Cell>
    <Cell><Data ss:Type="String">IDH3G, UQCRH, MRPL4 and ACADSB, as well as cellular redox regulation (GSR) (Fig. 3B), explaining enrichment for the functional terms mitochondrion,metabolic pathways,and oxidation-reduction process in the NPF group (Fig. 2)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31061140</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MRPS30</Data></Cell>
    <Cell><Data ss:Type="String">Novel breast cancer risk alleles and interaction with ionizing radiation among U.S. radiologic technologists</Data></Cell>
    <Cell><Data ss:Type="String">The radiation-associated breast cancer risk varied significantly by linked markers in 5p12 (rs930395, rs10941679, rs2067980 and rs4415084) in the mitochondrial ribosomal protein S30 (MRPS30) gene (P(interaction) = 0.04)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">20095854</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MRPS30</Data></Cell>
    <Cell><Data ss:Type="String">Genetic variants in the MRPS30 region and postmenopausal breast cancer risk</Data></Cell>
    <Cell><Data ss:Type="String">Combined main effect and intervention interaction analyses raise novel hypotheses concerning the MRPS30 genomic region and the effects of hormonal and dietary exposures on postmenopausal breast cancer risk</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21702935</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MRPS30</Data></Cell>
    <Cell><Data ss:Type="String">The 5p12 breast cancer susceptibility locus affects MRPS30 expression in estrogen-receptor positive tumors</Data></Cell>
    <Cell><Data ss:Type="String">The 5p12 risk allele affects MRPS30 expression in estrogen-responsive tumor cells after tumor initiation by a mechanism affecting chromatin availability</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24388359</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MRPS30</Data></Cell>
    <Cell><Data ss:Type="String">Evidence that the 5p12 Variant rs10941679 confers susceptibility to estrogen-receptor-positive breast cancer through FGF10 and MRPS30 regulation.</Data></Cell>
    <Cell><Data ss:Type="String">5p12 is mediated through coordinated activation of FGF10 and MRPS30, two candidate genes for breast cancer pathogenesis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27640304</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MRPS30</Data></Cell>
    <Cell><Data ss:Type="String">Integrative genomic analysis predicts causative cis-regulatory mechanisms of the breast cancer-associated genetic variant rs4415084</Data></Cell>
    <Cell><Data ss:Type="String">MRPS30 encodes a member of the mitochondrial ribosomal proteins, implicating the role of risk SNP in modulating mitochondrial activities in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29351903</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MTDH</Data></Cell>
    <Cell><Data ss:Type="String">Proteomic Profiling of Exosomes Secreted by Breast Cancer Cells with Varying Metastatic Potential</Data></Cell>
    <Cell><Data ss:Type="String">Presumably aid in targeting the primary cancer cells to specific metastatic sites</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29115712</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MTDH</Data></Cell>
    <Cell><Data ss:Type="String">MTDH Activation by 8q22 Genomic Gain Promotes Chemoresistance and Metastasis of Poor-Prognosis Breast Cancer</Data></Cell>
    <Cell><Data ss:Type="String">MTDH as an important therapeutic target for simultaneously enhancing chemotherapy efficacy and reducing metastasis risk</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19111877</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MTDH</Data></Cell>
    <Cell><Data ss:Type="String">Overexpression of metadherin/MTDH is associated with an aggressive phenotype and a poor prognosis in invasive breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">MTDH overexpression contributes to an aggressive phenotype, thus leading to a poor prognosis for primary invasive breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22903204</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MTDH</Data></Cell>
    <Cell><Data ss:Type="String">Knockdown of metadherin inhibits angiogenesis in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">MTDH is a viable therapeutic target for anti-angiogenesis in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25902416</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MTDH</Data></Cell>
    <Cell><Data ss:Type="String">Molecular Modification of Metadherin/MTDH Impacts the Sensitivity of Breast Cancer to Doxorubicin</Data></Cell>
    <Cell><Data ss:Type="String">MTDH gene plays a promoting role in the proliferation of breast cancer cells and its high expression may be associated with doxorubicin sensitivity of breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25993398</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MTDH</Data></Cell>
    <Cell><Data ss:Type="String">Epigenetic Activation of TWIST1 by MTDH Promotes Cancer Stem-like Cell Traits in Breast Cancer</Data></Cell>
    <Cell><Data ss:Type="String">MTDH promotes CSC accumulation and breast tumorigenicity by regulating TWIST1, deepening the understanding of MTDH function in cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26141861</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MTDH</Data></Cell>
    <Cell><Data ss:Type="String">Efficient and tumor-specific knockdown of MTDH gene attenuates paclitaxel resistance of breast cancer cells both in vivo and in vitro</Data></Cell>
    <Cell><Data ss:Type="String">NP-based co-delivery approach can effectively knock down the MTDH gene both in vitro and in vivo, which dramatically inhibits breast tumor growth, achieving effective TAX chemotherapy treatment without overt side effects</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30227879</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">MTDH</Data></Cell>
    <Cell><Data ss:Type="String">Elevated expression of MTDH predicts better prognosis of locally advanced HER-2 positive breast cancer patients receiving neoadjuvant chemotherapy plus trastuzumab</Data></Cell>
    <Cell><Data ss:Type="String">High MTDH expression was closely correlated with poor prognosis of patients and was an important factor affecting tumor progression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31490377</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">NANOG</Data></Cell>
    <Cell><Data ss:Type="String">Exosomes enriched in stemness/metastatic-related mRNAS promote oncogenic potential in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Stemness markers and enhance proliferation,migration and invasion abilities of neighboring cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">26528758</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">NANOG</Data></Cell>
    <Cell><Data ss:Type="String">RNA interference-mediated silencing of NANOG reduces cell proliferation and induces G0/G1 cell cycle arrest in breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">NANOG protein can bind to the promoter region of cyclinD1 and regulate cells cycle</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22381696</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">NANOG</Data></Cell>
    <Cell><Data ss:Type="String">Prognostic significance of NANOG and KLF4 for breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Strong expression of NANOG is an indicator of a poor prognosis for breast cancer patients, whereas KLF4 is a favorable prognostic indicator</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22528804</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">NANOG</Data></Cell>
    <Cell><Data ss:Type="String">Prognostic significance of NANOG and KLF4 for breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">NANOG stimulates the growth and metastasis of breast cancer cells, whereas KLF4 inhibits these processes.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22528804</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">NANOG</Data></Cell>
    <Cell><Data ss:Type="String">The pluripotency factor nanog promotes breast cancer tumorigenesis and metastasis</Data></Cell>
    <Cell><Data ss:Type="String">The involvement of Nanog in breast cancer metastasis, and provide the basis for the reported correlation between Nanog expression and poor prognosis of human breast cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23770853</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">NANOG</Data></Cell>
    <Cell><Data ss:Type="String">The pluripotency factor nanog promotes breast cancer tumorigenesis and metastasis</Data></Cell>
    <Cell><Data ss:Type="String">Nanog promotes the migration and invasion of breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23770853</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">NANOG</Data></Cell>
    <Cell><Data ss:Type="String">PD-1 promotes OCT4 and Nanog expression in breast cancer stem cells by sustaining PI3K/AKT pathway activation</Data></Cell>
    <Cell><Data ss:Type="String">PD-1 positive effect on OCT-A and Nanog was dependent on AKT activation</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28614911</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">NANOG</Data></Cell>
    <Cell><Data ss:Type="String">Immunohistochemical Expression of Nanog and Its Relation with Clinicopathologic Characteristics in Breast Ductal Carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">Nanog is a biomarker for prognostic prediction in patients with breast cancer. However, further studies of Nanog are suggested to provide novel therapeutic targets for curing breast cance</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30220190</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">NEUROD1</Data></Cell>
    <Cell><Data ss:Type="String">Exosomes enriched in stemness/metastatic-related mRNAS promote oncogenic potential in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Stemness markers and enhance proliferation,migration and invasion abilities of neighboring cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">26528758</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">NEUROD1</Data></Cell>
    <Cell><Data ss:Type="String">Methylated NEUROD1 promoter is a marker for chemosensitivity in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">NEUROD1 methylation is a chemosensitivity marker in estrogen receptor-negative breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">18519782</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">NEUROD1</Data></Cell>
    <Cell><Data ss:Type="String">DNA methylation of polycomb group target genes in cores taken from breast cancer centre and periphery</Data></Cell>
    <Cell><Data ss:Type="String">NEUROD1 was one of the genes that did not show statistically significant differences in the methylation levels between TUC and TUP, suggesting it is homogeneously methylated within the tumour.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19353266</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">NEUROD1</Data></Cell>
    <Cell><Data ss:Type="String">Whole genome DNA methylation signature of HER2-positive breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Top candidate biomarker genes are involved in transcription (HIST1H4, NEUROD1, IRF4, mir129, FOXC2, POU4F1),?neural signaling/development/differentiation (GABRA4, INA, NEUROD1, WDR69, POU4F1),?glucose metabolism (AKR1B1),?and epidermal growth factor signaling (CDKL2)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25089541</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">NEUROD1</Data></Cell>
    <Cell><Data ss:Type="String">Multigene methylation analysis of enriched circulating tumor cells associates with poor progression-free survival in metastatic breast cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">For following genes assays were designed using the Pyromark Assay Design Software Version 2 (Qiagen): AKR1B1, BMP6, CST6, HOXB4, HIST1H3C, ITIH5, NEUROD1, RASSF1, SOX17. All of these genes have been previously shown to be hypermethylated in breast cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29190932</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">NEUROD1</Data></Cell>
    <Cell><Data ss:Type="String">MiR-29b-1-5p is altered in BRCA1 mutant tumours and is a biomarker in basal-like breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Analysis of possible targets for miR-29b-1-5p reveals that the top 4 targets, USP28, NEUROD1, LIN9 and WDR26 have all been previously associated with breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30323900</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">NOC2L</Data></Cell>
    <Cell><Data ss:Type="String">Genome-wide meta-analysis identifies five new susceptibility loci for pancreatic cancer</Data></Cell>
    <Cell><Data ss:Type="String">Expression quantitative trait locus analysis in three independent pancreatic data sets provides molecular support of?NOC2L?as a pancreatic cancer susceptibility gene</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29422604</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">NOC2L</Data></Cell>
    <Cell><Data ss:Type="String">Deconvolution of DNA methylation identifies differentially methylated gene regions on 1p36 across breast cancer subtypes</Data></Cell>
    <Cell><Data ss:Type="String">We identified nineteen differentially methylated gene regions (DMGRs) in early stage tumors across eleven genes (AGRN, C1orf170, FAM41C, FLJ39609, HES4, ISG15, KLHL17, NOC2L, PLEKHN1, SAMD11, WASH5P)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="String">?28912426</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">PIGR</Data></Cell>
    <Cell><Data ss:Type="String">Uterine stromal cell suppression of pIgR production by uterine epithelial cells in vitro: a mechanism for regulation of pIgR production</Data></Cell>
    <Cell><Data ss:Type="String">Stromal cells can provide a signal that leads to the regulation of pIgR production</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">9234210</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">PIGR</Data></Cell>
    <Cell><Data ss:Type="String">Characterization of the human polymeric immunoglobulin receptor(PIGR)3'UTR and differential expression of PIGR mRNA during colon tumorigenesis</Data></Cell>
    <Cell><Data ss:Type="String">The entire 1.8 kb 3'UTR of human PIGR, and found it to contain multiple repetitive elements as well as elements that could affect the processing and stability of PIGR mRNA</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">14631119</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">PIGR</Data></Cell>
    <Cell><Data ss:Type="String">Expression and prognostic significance of the polymeric immunoglobulin receptor in epithelial ovarian cancer</Data></Cell>
    <Cell><Data ss:Type="String">High tumour-specific expression of PIGR was found to be associated with a favourable prognosis in unadjusted, but not in adjusted, analysis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24568264</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">PIGR</Data></Cell>
    <Cell><Data ss:Type="String">Polymeric immunoglobulin receptor expression is predictive of poor prognosis in glioma patients</Data></Cell>
    <Cell><Data ss:Type="String">PIgR could be a novel predictor for poor prognosis of patients with glioma after surgical resection</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25232405</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">PIGR</Data></Cell>
    <Cell><Data ss:Type="String">Exploitation of the Polymeric Immunoglobulin Receptor for Antibody Targeting to Renal Cyst Lumens in Polycystic Kidney Disease</Data></Cell>
    <Cell><Data ss:Type="String">PIgR-mediated transcytosis of antagonistic antibodies in dIgA format can be exploited for targeted therapy in ADPKD</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25922073</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">PIK3R5</Data></Cell>
    <Cell><Data ss:Type="String">Analysis of molecular markers as predictive factors of lymph node involvement in breast carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">The PIK3R5 gene serves a role in cell growth, differentiation, proliferation, motility, survival and intracellular transport, and its route is associated with the progression of melanoma. The PIK3R5 gene is associated with inhibition of autophagy (promoting tumor growth) and certain authors have suggested that autophagy also works as a cytoprotective mechanism.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28123587</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">PKN2</Data></Cell>
    <Cell><Data ss:Type="String">Protein kinase C inhibitor chelerythrine selectively inhibits proliferation of triple-negative breast cancer cells.</Data></Cell>
    <Cell><Data ss:Type="String">PKN2, one of the PKC subtypes, was highly expressed in TNBC cell lines, and knocking down PKN2 in TNBC cells inhibited colony formation and xenograft growth. This indicates that PKN2 is required for the survival of TNBC cells, and could be the target mediates the selective activity of chelerythrine.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28515445</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">PKN2</Data></Cell>
    <Cell><Data ss:Type="String">PKN2 in colon cancer cells inhibits M2 phenotype polarization of tumor-associated macrophages via regulating DUSP6-Erk1/2 pathway</Data></Cell>
    <Cell><Data ss:Type="String">The expression of PKN2 in colon cancer cells predicted a favorable prognosis and was associated with low M2 macrophage content in human colon cancer tissues.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29368606</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">PKN2</Data></Cell>
    <Cell><Data ss:Type="String">PKN2 in colon cancer cells inhibits M2 phenotype polarization of tumor-associated macrophages via regulating DUSP6-Erk1/2 pathway</Data></Cell>
    <Cell><Data ss:Type="String">PKN2 suppresses the expression of IL4 and IL10 from colon cancer cells by inhibiting Erk1/2 phosphorylation, which is required for phosphorylation and binding of CREB and Elk-1 to the promoters of IL4 and IL10. DUSP6, which is phosphorylated and activated through direct association with PKN2, suppresses Erk1/2 activation.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29368606</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">Plau</Data></Cell>
    <Cell><Data ss:Type="String">Proteomic Profiling of Exosomes Secreted by Breast Cancer Cells with Varying Metastatic Potential</Data></Cell>
    <Cell><Data ss:Type="String">Presumably aid in targeting the primary cancer cells to specific metastatic sites</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29115712</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">Plau</Data></Cell>
    <Cell><Data ss:Type="String">Transcriptional complexity and roles of Fra-1/AP-1 at the uPA/Plau locus in aggressive breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">We unveil a heretofore-unsuspected transcriptional complexity at Plau in a reference metastatic breast cancer cell line with pleiotropic effects for Fra-1, providing novel information on AP-1 transcriptional action</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25200076</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">Plau</Data></Cell>
    <Cell><Data ss:Type="String">Gene Expression Signatures in Circulating Tumor Cells Correlate with Response to Therapy in Metastatic Breast Cancer</Data></Cell>
    <Cell><Data ss:Type="String">Fourteen genes were identified as significantly differentially expressed between CTC+ and CTC- patients (KRT19, FLT1, EGFR, EPCAM, GZMM, PGR, CD24, KIT, PLAU, ALDH1A1, CTSD, MKI67, TWIST1, and ERBB2). KRT19 was highly expressed in CTC+ patients and ADAM17 in the NR at TP1</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28778937</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">Plau</Data></Cell>
    <Cell><Data ss:Type="String">HMGA1 regulates the Plasminogen activation system in the secretome of breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">From an inspection of the HMGA1-dependent secreted factors it turned out that HMGA1 influences the presence in the extra cellular milieu of key components of the Plasminogen activation system (PLAU, SERPINE1, and PLAUR) that has a prominent role in promoting metastasis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28924209</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">Plau</Data></Cell>
    <Cell><Data ss:Type="String">Transcriptomic pathway analysis of urokinase receptor silenced breast cancer cells: a microarray study</Data></Cell>
    <Cell><Data ss:Type="String">Transcriptomic changes and predicted pathways supported and consolidated some of the earlier understanding in the context of PLAUR signaling; including our recent observations in DNA damage and repair process. In addition, we have identified several novel pathways where PLAUR is implicated</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29254187</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">Plau</Data></Cell>
    <Cell><Data ss:Type="String">Fluid shear stress stimulates breast cancer cells to display invasive and chemoresistant phenotypes while upregulating PLAU in a 3D bioreactor</Data></Cell>
    <Cell><Data ss:Type="String">Pulsatile shear stress promotes breast cancer cell proliferation, invasive potential, chemoresistance, and PLAU signaling</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31317530</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">PLCB4</Data></Cell>
    <Cell><Data ss:Type="String">Deep sequencing of uveal melanoma identifies a recurrent mutation in PLCB4</Data></Cell>
    <Cell><Data ss:Type="String">PLCB4 hotspot mutation is similarly a gain-of-function mutation leading to activation of the same signaling pathway, promoting UM tumorigenesis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26683228</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">PLCB4</Data></Cell>
    <Cell><Data ss:Type="String">PLCB4 copy gain and PLC4 overexpression in primary gastrointestinal stromal tumors: Integrative characterization of a lipid-catabolizing enzyme associated with worse disease-free survival</Data></Cell>
    <Cell><Data ss:Type="String">YAP1 increased PLCB4 mRNA and protein expression, and both molecules significantly promoted cell proliferation</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28212550</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">PLCB4</Data></Cell>
    <Cell><Data ss:Type="String">RNA Sequencing Uncovers Molecular Mechanisms Underlying Pathological Complete Response to Chemotherapy in Patients with Operable Breast Cancer</Data></Cell>
    <Cell><Data ss:Type="String">We found key genes that may contribute to pCR to chemotherapy, such as PLCB4, ADCY6, and CNR1, as well as some transcription factors</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28880852</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">PLCB4</Data></Cell>
    <Cell><Data ss:Type="String">Diagnostic and prognostic value of mRNA expression of phospholipase C β family genes in hepatitis B virus?associated hepatocellular carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">Validation using GEPIA revealed that PLCB1 and PLCB2 were associated with OS and PLCB1 and PLCB4 were associated with RFS</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30896816</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">PLCB4</Data></Cell>
    <Cell><Data ss:Type="String">Distinct Prognostic Values of Phospholipase C Beta Family Members for Non-Small Cell Lung Carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">PLCB1, PLCB2, PLCB3, and PLCB4 appear to be potential biomarkers for the prognosis of patients with NSCLC</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31080817</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">POLR2K</Data></Cell>
    <Cell><Data ss:Type="String">Identification of Potential Driver Genes in Human Liver Carcinoma by Genomewide Screening</Data></Cell>
    <Cell><Data ss:Type="String">Of the 11 genes, 5 siRNAs for SCRIB, NCSTN, HSF1, TATDN1, and POLR2K significantly reduced the viability of both HepG2 and HuH-7 liver cancer cell lines</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19366792</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">POLR2K</Data></Cell>
    <Cell><Data ss:Type="String">An integrative genomic and transcriptomic analysis reveals molecular pathways and networks regulated by copy number aberrations in basal-like, HER2 and luminal cancers</Data></Cell>
    <Cell><Data ss:Type="String">In HER2 cancers, the nucleotide Excision Repair Pathway was significantly enriched for genes whose expression correlates with copy number (P = 0.0214), with recurrent gains and amplifications of POLR2K and losses of RPA2 </Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19688261</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">POLR2K</Data></Cell>
    <Cell><Data ss:Type="String">The role of tumor metabolism as a driver of prostate cancer progression and lethal disease: results from a nested case-control study</Data></Cell>
    <Cell><Data ss:Type="String">Oxidative phosphorylation and pyrimidine metabolism were identified as the most dysregulated pathways in lethal tumors (p&lt;0.007), and within these pathways, a number of novel differentially expressed genes were identified including?POLR2K?and?APT6V1A</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27980733</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">POLR2K</Data></Cell>
    <Cell><Data ss:Type="String">Identification of miRNA biomarkers of pneumonia using RNA sequencing and bioinformatics analysis</Data></Cell>
    <Cell><Data ss:Type="String">POLR2K and APP were predicted targets of has-let-7f-1. The results of the present study demonstrated that has-let-7f-1 may serve a role in the development of cancer and the Notch signaling pathway</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28413462</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">POSTN</Data></Cell>
    <Cell><Data ss:Type="String">Periostin is identified as a putative metastatic marker in breast cancer-derived exosomes</Data></Cell>
    <Cell><Data ss:Type="String">Periostin as a protein that is enriched in exosomes secreted by metastatic cells and validated its presence in a pilot cohort of breast cancer patient samples with localized disease or lymph node (LN) metastasis</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">27589561</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">POSTN</Data></Cell>
    <Cell><Data ss:Type="String">Cancer Stem Cell-Related Gene Periostin: A Novel Prognostic Marker for Breast Cancer</Data></Cell>
    <Cell><Data ss:Type="String">Periostin was found to be related to the CSC and an independent prognostic factor for breast cancer. It is also perhaps a potential target to breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23056395</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">POSTN</Data></Cell>
    <Cell><Data ss:Type="String">Periostin expression in cancer-associated fibroblasts of invasive ductal breast carcinoma.</Data></Cell>
    <Cell><Data ss:Type="String">POSTN might be a factor playing an important role in the mechanism of IDC progression.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27633896</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">POSTN</Data></Cell>
    <Cell><Data ss:Type="String">Expression of periostin in breast cancer cells.</Data></Cell>
    <Cell><Data ss:Type="String">POSTN expression in the cytoplasm of IDC cancer cells may play an important role in cancer transformation mechanism.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28902360</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">POSTN</Data></Cell>
    <Cell><Data ss:Type="String">Epithelial periostin expression is correlated with poor survival in patients with invasive breast carcinoma.</Data></Cell>
    <Cell><Data ss:Type="String">Periostin may play an important role in the progression of breast tumor, and epithelial periostin expression may serve as a new parameter for prediction of prognosis in patients with invasive breast carcinoma(IBC).</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29161296</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">POU4F1</Data></Cell>
    <Cell><Data ss:Type="String">AML1/ETO proteins control POU4F1/BRN3A expression and function in t(8;21) acute myeloid leukaemia</Data></Cell>
    <Cell><Data ss:Type="String">POU4F1/BRN3A as a novel potential up-regulated AML1/ETO target gene whose dramatically high expression may co-operate with AML1/ETO in t(8;21) cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">20460523</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">POU4F1</Data></Cell>
    <Cell><Data ss:Type="String">Genome-wide methylation screen in low-grade breast cancer identifies novel epigenetically altered genes as potential biomarkers for tumor diagnosis</Data></Cell>
    <Cell><Data ss:Type="String">In tumors, median methylation levels of BCAN, HOXD1, KCTD8, KLF11, NXPH1, POU4F1, SIM1, and TCF7L1 were 30% higher than in normal samples, representing potential biomarkers for tumor diagnosis</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22930747</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">POU4F1</Data></Cell>
    <Cell><Data ss:Type="String">DNA methylation in ductal carcinoma in situ of the breast</Data></Cell>
    <Cell><Data ss:Type="String">Eleven genes (BCAN, HOXD1, KCTD8, KLF11, NXPH1, PCDH10, POU4F1, RYR2, SIM1, TAC1, and TCF7L1) were validated as being aberrantly methylated in DCIS and IDC compared with normal breast tissue</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23826974</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">POU4F1</Data></Cell>
    <Cell><Data ss:Type="String">POU4F1 is associated with t(8;21) acute myeloid leukemia and contributes directly to its unique transcriptional signature</Data></Cell>
    <Cell><Data ss:Type="String">Among the most highly differentially expressed genes, half are known AML1/ETO targets, implying that the unique transcriptional signature of t(8;21) AML is, in part, attributable to POU4F1 and not AML1/ETO?itself.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="String">?20376082</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">PRPF3</Data></Cell>
    <Cell><Data ss:Type="String">An integrative analysis of colon cancer identifies an essential function for PRPF6 in tumor growth</Data></Cell>
    <Cell><Data ss:Type="String">Knockdown of the tri-snRNP protein PRPF31, PRPF8, BRR2, or PRPF3 in colon cancer cells led to reduced growth specifically in cell lines that expressed high levels of PRPF6?</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24788092</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">PSMC5</Data></Cell>
    <Cell><Data ss:Type="String">A network-based, integrative study to identify core biological pathways that drive breast cancer clinical subtypes</Data></Cell>
    <Cell><Data ss:Type="String">Several seed genes for the ER network, including APPBP2, ASH2L, BAG4, CCND1, CLTC, DDX5, DEDD, EPN3, GPAA1, PHB, PRKAR1A, PRKDC, PSMC5, PTK2, RPS6KB1, SPOP, and YWHAZ were not significantly over- or under-expressed in ER+ cancers relative to other subtypes but showed copy number abnormalities</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22343619</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">PSMC5</Data></Cell>
    <Cell><Data ss:Type="String">Radiosensitizing effect of PSMC5, a 19S proteasome ATPase, in H460 lung cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">PSMC5 facilitates the damaging effects of radiation in radiation-responsive H460 cancer cells and therefore may serve as a prognostic indicator for radiotherapy and molecular targeted therapy in lung cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26592665</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">PSMC5</Data></Cell>
    <Cell><Data ss:Type="String">Using Quantitative Seroproteomics to Identify Antibody Biomarkers in Pancreatic Cancer</Data></Cell>
    <Cell><Data ss:Type="String">We further interrogated these proteins in over 80 GVAX-treated patients' pancreases and uniformly found a significant increase in the expression of MYPT1, PSMC5, and TFRC in neoplastic compared with non-neoplastic pancreatic ductal epithelium</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26842750</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">PSMC5</Data></Cell>
    <Cell><Data ss:Type="String">Circulating protein and antibody biomarker for personalized cancer immunotherapy</Data></Cell>
    <Cell><Data ss:Type="String">Using this assay, several new tumor antigens (MYPT1, PSMC5 and TRFR) were identified that were found to have significantly different expression in tumors compared with normal tissue</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27532021</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">PSMD2</Data></Cell>
    <Cell><Data ss:Type="String">PSMD2 regulates breast cancer cell proliferation and cell cycle progression by modulating p21 and p27 proteasomal degradation</Data></Cell>
    <Cell><Data ss:Type="String">Upregulated PSMD2 is a valuable predictor for clinical outcomes in BC and may have an essential role in BC tumorigenesis.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29777785</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">PSMD2</Data></Cell>
    <Cell><Data ss:Type="String">PSMD2 regulates breast cancer cell proliferation and cell cycle progression by modulating p21 and p27 proteasomal degradation</Data></Cell>
    <Cell><Data ss:Type="String">Transcriptome signatures involving proliferation, cell cycle, and apoptosis were critically enriched in specimens with elevated PSMD2. Consistently, PSMD2 knockdown inhibited cell proliferation and arrested cell cycle at G0/G1 phase in vitro, as well as suppressed tumor growth in vivo.The cell cycle arrest caused by silencing PSMD2 partially resulted from increased p21 and/or p27. Mechanically, PSMD2 physically interacted with p21 and p27 and mediated their ubiquitin-proteasome degradation with the cooperation of USP14.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29777785</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RAB13</Data></Cell>
    <Cell><Data ss:Type="String">Characterization of RNA in exosomes secreted by human breast cancer cell lines using next-generation sequencing</Data></Cell>
    <Cell><Data ss:Type="String">RAB13 distinguish exosomes produced by low metastatic breast cancer cell line (MDA-MB-436) from that produced by highly metastatic breast cancer cell line (MDA-MB-231)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">24255815</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RAB13</Data></Cell>
    <Cell><Data ss:Type="String">Rab35 promotes the recruitment of Rab8, Rab13 and Rab36 to recycling endosomes through MICAL-L1 during neurite outgrowth</Data></Cell>
    <Cell><Data ss:Type="String">We further showed by functional ablation experiments that each of these downstream Rabs regulates neurite outgrowth in a non-redundant manner downstream of Rab35 and MICAL-L1, e.g. by showing that knockdown of Rab36 inhibited recruitment of Rab36-specific effector JIP4 to Arf6-positive recycling endosomes, and caused inhibition of neurite outgrowth without affecting accumulation of Rab8 and Rab13 in the same Arf6-positive area</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25086062</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RAB13</Data></Cell>
    <Cell><Data ss:Type="String">DENND2B activates Rab13 at the leading edge of migrating cells and promotes metastatic behavior</Data></Cell>
    <Cell><Data ss:Type="String">Blocking Rab13 activation by DENND2B may provide a novel target to limit the spread of epithelial cancers</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25713415</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RAB13</Data></Cell>
    <Cell><Data ss:Type="String">Regulation of Cancer Cell Behavior by the Small GTPase Rab13</Data></Cell>
    <Cell><Data ss:Type="String">Rabs have been implicated in all steps of membrane trafficking ranging from vesicle formation and transport to vesicle docking/tethering and fusion. Vesicle trafficking controls the localization and levels of a myriad of proteins, thus regulating cellular functions including proliferation, metabolism, cell-cell adhesion, and cell migration</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27044746</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RAB13</Data></Cell>
    <Cell><Data ss:Type="String">Overexpression of MICAL2, a novel tumor-promoting factor, accelerates tumor progression through regulating cell proliferation and EMT</Data></Cell>
    <Cell><Data ss:Type="String">Rab13 is activated by its effector MICAL-L2 to recruit actin-binding proteins to promote migrating cell</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29483957</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RAB13</Data></Cell>
    <Cell><Data ss:Type="String">RAB13 as a novel prognosis marker promotes proliferation and chemotherapeutic resistance in gastric cancer</Data></Cell>
    <Cell><Data ss:Type="String">RAB13 promotes the proliferation and confers CDDP and 5-FU resistance to GC cells, which provides experimental support to target this protein in future clinical practice</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31474334</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RANBP1</Data></Cell>
    <Cell><Data ss:Type="String">Ran-binding protein 1 (RanBP1) forms a ternary complex with Ran and karyopherin beta and reduces Ran GTPase-activating protein (RanGAP) inhibition by karyopherin beta</Data></Cell>
    <Cell><Data ss:Type="String">RanBP1 and karyopherin β interact with distinct sites of Ran and suggest that RanBP1 plays an essential role in nuclear transport by permitting RanGAP-mediated hydrolysis of GTP on Ran complexed to karyopherin β</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">8995296</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RANBP1</Data></Cell>
    <Cell><Data ss:Type="String">RANBP1 localizes a subset of mitotic regulatory factors on spindle microtubules and regulates chromosome segregation in human cells</Data></Cell>
    <Cell><Data ss:Type="String">RANBP1 activity is required for the proper localization of specific factors that regulate microtubule function; loss of this activity contributes to the generation of aneuploidy in a microtubule-dependent manner</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">17940066</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RANBP1</Data></Cell>
    <Cell><Data ss:Type="String">RanBP1 downregulation sensitizes cancer cells to taxol in a caspase-3-dependent manner</Data></Cell>
    <Cell><Data ss:Type="String">RanBP1-interfered cells show an increased apoptotic response to taxol compared to their counterpart with normal or high RanBP1 levels, and this response is caspase-3 dependent</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19270727</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RANBP1</Data></Cell>
    <Cell><Data ss:Type="String">Sgk1 enhances RANBP1 transcript levels and decreases taxol sensitivity in RKO colon carcinoma cells</Data></Cell>
    <Cell><Data ss:Type="String">SGK1 also affects mitotic stability in colon carcinoma cells by regulating the expression of RANBP1 (Ran-specific binding protein 1), the pivotal regulator of GTPase RAN. SGK1 modulates RAN/RANBP1 abundance at the transcriptional level via SP1 activation and phosphorylation on Serine 59, thus affecting taxol sensitivity in these cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23108393</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RANBP1</Data></Cell>
    <Cell><Data ss:Type="String">Distinct RanBP1 nuclear export and cargo dissociation mechanisms between fungi and animals</Data></Cell>
    <Cell><Data ss:Type="String">The key feature for the two mechanistic changes from fungi to animals was the loss of affinity between RanBP1-RanGTP and CRM1, since residues mediating their interaction in fungi were not conserved in animals</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31021318</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RBM10</Data></Cell>
    <Cell><Data ss:Type="String">mRNA expression of the putative antimetastatic gene BRMS1 and of apoptosis-related genes in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">A significant (p=0.03) inverse correlation between BRMS1 mRNA expression and expression of the mRNA corresponding to the large variant of the X-chromosome RBM10 gene was found</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21737612</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RBM10</Data></Cell>
    <Cell><Data ss:Type="String">RBM5, 6, and 10 Differentially Regulate NUMB Alternative Splicing to Control Cancer Cell Proliferation</Data></Cell>
    <Cell><Data ss:Type="String">RBM10 mutations identified in lung cancer cells disrupt NUMB splicing regulation to promote cell growth</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24332178</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RBM10</Data></Cell>
    <Cell><Data ss:Type="String">Functional analysis reveals that RBM10 mutations contribute to lung adenocarcinoma pathogenesis by deregulating splicing</Data></Cell>
    <Cell><Data ss:Type="String">Changes in proliferation rates of LUAD-derived cells caused by these RBM10 missense mutants correlated with alterations in RNA splicing of?RBM10?target genes</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28091594</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RBM10</Data></Cell>
    <Cell><Data ss:Type="String">Expression of RNA-binding motif 10 is associated with advanced tumor stage and malignant behaviors of lung adenocarcinoma cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">RNA-binding motif 10 regulates many gene pathways involving in the tumor development or progression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28347232</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RBM10</Data></Cell>
    <Cell><Data ss:Type="String">Increased cell apoptosis in human lung adenocarcinoma and in vivo tumor growth inhibition by RBM10, a tumor suppressor gene</Data></Cell>
    <Cell><Data ss:Type="String">The accumulated and stable overexpression of RBM10 in the xenograft BALB/c nude mice model significantly inhibited the tumor growth rate</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29085465</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RHO</Data></Cell>
    <Cell><Data ss:Type="String">Rhodopsin and retinoblastoma. A monoclonal antibody histopathologic study</Data></Cell>
    <Cell><Data ss:Type="String">Some well-differentiated retinoblastomas express both rhodopsin and S-antigen, and as such express proteins that participate in the initial events in the phototransduction of visio</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">3942531</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RHO</Data></Cell>
    <Cell><Data ss:Type="String">Mechanisms of photoreceptor cell death in cancer-associated retinopathy</Data></Cell>
    <Cell><Data ss:Type="String">These observations suggest that anti-recoverin antibody is incorporated into rod photoreceptor cells and modulates rhodopsin phosphorylation, which in turn produces activation of caspase-dependent apoptotic pathways</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">11222531</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RHO</Data></Cell>
    <Cell><Data ss:Type="String">Photoreceptor proteins as cancer-retina antigens</Data></Cell>
    <Cell><Data ss:Type="String">Melanocytes also express mRNA of all photoreceptor genes besides transducin, but were devoid of the corresponding protein, which was tested for rhodopsin, cGMP-phosphodiesterase, guanylyl cyclase and recoverin</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">17187367</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RIPK1</Data></Cell>
    <Cell><Data ss:Type="String">RIPK1 Binds MCU to Mediate Induction of Mitochondrial Ca2+ Uptake and Promotes Colorectal Oncogenesis</Data></Cell>
    <Cell><Data ss:Type="String">These findings identify the RIPK1-MCU pathway as a promising target to treat colorectal cancer.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29531160</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RIPK1</Data></Cell>
    <Cell><Data ss:Type="String">Differential involvement of TAK1, RIPK1 and NF-κB signaling in Smac mimetic-induced cell death in breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">TAK1, receptor-interacting kinase 1 (RIPK1) as well as canonical and non-canonical NF-κB signaling are differentially involved in SM-induced cell death in breast cancer cells. These findings contribute to a better understanding of SM-induced signaling pathways</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30391931</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RIPK1</Data></Cell>
    <Cell><Data ss:Type="String">FKBP12 mediates necroptosis by initiating RIPK1-RIPK3-MLKL signal transduction in response to TNF receptor 1 ligation</Data></Cell>
    <Cell><Data ss:Type="String">FKBP12 may target RIPK1 and RIPK3 to mediate necroptosis in vitro and in vivo Collectively, our data demonstrate that FKBP12 could be a potential therapeutic target for the clinical treatment of necroptosis-associated diseases</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31028177</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RIPK1</Data></Cell>
    <Cell><Data ss:Type="String">Discovery of potent necroptosis inhibitors targeting RIPK1 kinase activity for the treatment of inflammatory disorder and cancer metastasis</Data></Cell>
    <Cell><Data ss:Type="String">PK68 is a potent and selective inhibitor of RIPK1 and also highlights its great potential for use in the treatment of inflammatory disorders and cancer metastasis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31235688</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RN7SL1</Data></Cell>
    <Cell><Data ss:Type="String">Exosome RNA Unshielding Couples Stromal Activation to Pattern Recognition Receptor Signaling in Cancer</Data></Cell>
    <Cell><Data ss:Type="String">Unshielded RN7SL1 in exosomes acts as a DAMP and activates breast cancer RIG-I to promote aggressive features of cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">28709002</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RN7SL1</Data></Cell>
    <Cell><Data ss:Type="String">Exosomal proteins as potential markers of tumor diagnosis</Data></Cell>
    <Cell><Data ss:Type="String">Breast cancer cells can stimulate stromal fibroblasts to produce stromal exosomes, which contain unshielded endogenous RNA (RN7SL1), via triggering NOTCH-MYC pathways. Delivering unshielded RN7SL1 to breast cancer cells facilitates cancer growth, metastasis, and therapy resistance through retinoic acid-inducible gene I (RIG-I) signaling</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29282096</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RN7SL1</Data></Cell>
    <Cell><Data ss:Type="String">The decade of exosomal long RNA species: an emerging cancer antagonist</Data></Cell>
    <Cell><Data ss:Type="String">Assessments of the blood samples of breast cancer patients revealed the presence of unshielded RN7SL1 in exosomes. Thus, exosomal content can be utilized to identify patients with more aggressive cancers by detecting exosome-binding RN7SL1</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29558960</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RN7SL1</Data></Cell>
    <Cell><Data ss:Type="String">Exosomes From The Tumor Microenvironment Promote Breast Cancer Progression And Therapy Resistance Through Unshielded Non-Coding Rna</Data></Cell>
    <Cell><Data ss:Type="String">Unshielded stromal RN7SL1 in exosomes, which is also found in cancer patients, is transferred to breast cancer cells to stimulate the pattern recognition receptor RIG-I and activate STAT1-dependent anti-viral signaling</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RPL26L1</Data></Cell>
    <Cell><Data ss:Type="String">Patterns of ribosomal protein expression specify normal and malignant human cells</Data></Cell>
    <Cell><Data ss:Type="String">Among these, RPL26L1 and RPS27L were exclusively up-regulated in breast and thyroid carcinomas, respectively, whereas RPL21 had decreased expression in breast and uterine cancers</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27884178</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RPL26L1</Data></Cell>
    <Cell><Data ss:Type="String">Comparative Analysis of Gene Expression Status to Predict Response to Initial Multiple Myeloma Treatment: Utility of the Mmrf Commpass Database in Validating Historical Findings</Data></Cell>
    <Cell><Data ss:Type="String">In the IMiD-based cohort, C14orf2 and RPL26L1 were significantly increased in responders (n=32) vs. non-responders (n=7, p&lt;0.05). In the PI+IMiD treatment group, ACVC1C, CRYGS, FUNDC1, PSMB3, RPL26L1, HIST1H3B, PSMB10 and STUB1?were significantly increased whereas TMC8, MAPK4, CCNB1IP1, SAP18, ANK3, JAK1, RUNX3, IKZF1, CUL4B, HNRNPC and WIPF2 were significantly decreased in responders (n=361) vs. non-responders (n=18) (p&lt;0.05-&lt;0.001)</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RPL28</Data></Cell>
    <Cell><Data ss:Type="String">Characterization of RNA in exosomes secreted by human breast cancer cell lines using next-generation sequencing</Data></Cell>
    <Cell><Data ss:Type="String">RPL28 distinguish exosomes produced by low metastatic breast cancer cell line (MDA-MB-436) from that produced by highly metastatic breast cancer cell line (MDA-MB-231)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">24255815</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RPL28</Data></Cell>
    <Cell><Data ss:Type="String">Long non-coding RNA GAS5 and ZFAS1 are prognostic markers involved in translation targeted by miR-940 in prostate cancer</Data></Cell>
    <Cell><Data ss:Type="String">GAS5 and ZFAS1 are targeted by miR-940 via NAA10 and RPL28</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29416676</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RPL28</Data></Cell>
    <Cell><Data ss:Type="String">Ribosomal Proteins Regulate MHC Class I Peptide Generation for Immunosurveillance</Data></Cell>
    <Cell><Data ss:Type="String">Depleting RPL6 decreases ubiquitin-dependent peptide presentation, whereas depleting RPL28 increases ubiquitin-dependent and -independent peptide presentation</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30712990</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RPL28</Data></Cell>
    <Cell><Data ss:Type="String">Germline variability and tumor expression level of ribosomal protein gene?RPL28?are associated with survival of metastatic colorectal cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">Repression of RPL28 reduced proliferation by 1.4-fold to 5.6-fold (P &lt; 0.05) in colon cancer HCT116 and HT-29 cells. Our findings suggest that the ribosomal RPL28 protein may influence mCRC outcome</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31506518</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RPPH1</Data></Cell>
    <Cell><Data ss:Type="String">Characterization of RNA in exosomes secreted by human breast cancer cell lines using next-generation sequencing</Data></Cell>
    <Cell><Data ss:Type="String">RPPH1 distinguish exosomes produced by low metastatic breast cancer cell line (MDA-MB-436) from that produced by highly metastatic breast cancer cell line (MDA-MB-231)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">24255815</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RPPH1</Data></Cell>
    <Cell><Data ss:Type="String">Inhibition of breast cancer cell proliferation and tumorigenesis by long non-coding RNA?RPPH1?down-regulation of miR-122 expression</Data></Cell>
    <Cell><Data ss:Type="String">Breast cancer progression can be promoted by directly targeting miR-122 through lncRNA RPPH1</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29200969</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RPS10</Data></Cell>
    <Cell><Data ss:Type="String">Morin suppresses cachexia-induced muscle wasting by binding to ribosomal protein S10 in carcinoma cells</Data></Cell>
    <Cell><Data ss:Type="String">Morin indirectly prevents muscle wasting induced by cancer cachexia by suppressing cancer growth via binding to RPS10</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30389140</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">RPS10</Data></Cell>
    <Cell><Data ss:Type="String">Cancer-Associated Eukaryotic Translation Initiation Factor 1A Mutants Impair Rps3 and Rps10 Binding and Enhance Scanning of Cell Cycle Genes</Data></Cell>
    <Cell><Data ss:Type="String">These mutations diminished the eIF1A interaction with Rps3 and Rps10 implicated in scanning arrest</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30420357</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">S1PR2</Data></Cell>
    <Cell><Data ss:Type="String">The sphingosine 1-phosphate receptor 2 is shed in exosomes from breast cancer cells and is N-terminally processed to a short constitutively active form that promotes extracellular signal regulated kinase activation and DNA synthesis in fibroblasts.</Data></Cell>
    <Cell><Data ss:Type="String">S1P2 is released from breast cancer cells in exosomes and is processed by fibroblasts to promote ERK signaling and proliferation of breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">30034630</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">S1PR2</Data></Cell>
    <Cell><Data ss:Type="String">Tumor-suppressive sphingosine-1-phosphate receptor-2 counteracting tumor-promoting sphingosine-1-phosphate receptor-1 and sphingosine kinase 1 Jekyll Hidden behind Hyde</Data></Cell>
    <Cell><Data ss:Type="String">S1PR2 expressed in host endothelial cells and tumor-infiltrating myeloid cells in concert mediates potent inhibition of tumor angiogenesis and tumor growth?in vivo, with inhibition of VEGF expression and MMP9 activity</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21984966</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">S1PR2</Data></Cell>
    <Cell><Data ss:Type="String">Communication between host organism and cancer cells is transduced by systemic sphingosine kinase 1/sphingosine 1-phosphate signalling to regulate tumour metastasis</Data></Cell>
    <Cell><Data ss:Type="String">Local tumour growth is regulated by both S1P from the tumour and systemic S1P, whereas lung colonization and metastasis is selectively controlled via systemic S1P and downregulation of breast cancer metastasis suppressor 1 (BRMS1; a master suppressor of metastasis) through S1PR2 signalling</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22707406</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">S1PR2</Data></Cell>
    <Cell><Data ss:Type="String">The tumor suppressive TGF-β/SMAD1/S1PR2 signaling axis is recurrently inactivated in diffuse large B-cell lymphoma</Data></Cell>
    <Cell><Data ss:Type="String">Uncover an important novel tumor suppressive function of the TGF-β/TGF-βR2/SMAD1/S1PR2 axis in DLBCL, and show that DLBCL cells have evolved to inactivate the pathway at the level of SMAD1 expression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29615404</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">SDHA</Data></Cell>
    <Cell><Data ss:Type="String">SDHA is a tumor suppressor gene causing paraganglioma</Data></Cell>
    <Cell><Data ss:Type="String">SDHA gene should be added to the list of genes encoding tricarboxylic acid cycle proteins that act as tumor suppressor genes and can now be considered as a new paraganglioma/pheochromocytoma susceptibility gene</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">20484225</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">SDHA</Data></Cell>
    <Cell><Data ss:Type="String">Clinical Characterization of the Pheochromocytoma and Paraganglioma Susceptibility Genes?SDHA,?TMEM127,?MAX, and?SDHAF2?for Gene-Informed Prevention</Data></Cell>
    <Cell><Data ss:Type="String">The SDHA, TMEM127, MAX, and SDHAF2 genes may contribute to hereditary pheochromocytoma and paraganglioma</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28384794</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">SDHA</Data></Cell>
    <Cell><Data ss:Type="String">Germline SDHA mutations in children and adults with cancer</Data></Cell>
    <Cell><Data ss:Type="String">Immunohistochemical staining and assessment of patient tumors for second hits and loss of heterozygosity in SDHA confirmed GIST as an SDHA-associated tumor and suggests SDHA germline mutations may be a driver in neuroblastoma tumorigenesis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30068732</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">SDHA</Data></Cell>
    <Cell><Data ss:Type="String">Succinate dehydrogenase expression in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">Loss of SDHA or SDHB expression was observed in about 3% of breast cancers in this study. Low SDH expression status in breast tumor cells was associated with younger age at diagnosis and low-grade histology</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="String">?23888270</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">SF3A2</Data></Cell>
    <Cell><Data ss:Type="String">Spliceosome mutations in myelodysplastic syndromes and chronic myelomonocytic leukemia</Data></Cell>
    <Cell><Data ss:Type="String">SF3A2 is part of the U2 snRNP, and another member of this complex (SF3B1) is recurrently mutated in myelodysplastic syndrome, acute myeloid leukemia, and chronic lymphocytic leukemia</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23327988</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">SF3B4</Data></Cell>
    <Cell><Data ss:Type="String">Increased Copy Number of the Gene Encoding SF3B4 Indicates Poor Prognosis in Hepatocellular Carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">High SF3B4 expression is significantly associated with intrahepatic metastasis and poor prognosis</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27127115</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">SF3B4</Data></Cell>
    <Cell><Data ss:Type="String">Increased Copy Number of the Gene Encoding SF3B4 Indicates Poor Prognosis in Hepatocellular Carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">SF3B4 expression was significantly higher in cancerous than in non-cancerous tissues and positively correlated with SF3B4 DNA copy number</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27127115</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">SF3B4</Data></Cell>
    <Cell><Data ss:Type="String">Synchronous bilateral breast cancer in a patient with Nager syndrome</Data></Cell>
    <Cell><Data ss:Type="String">Somatic inactivating mutations of SF3B4 occur occasionally in breast cancer, and these findings support the idea that SF3B4 is a tumor suppressor</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28139434</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">SF3B4</Data></Cell>
    <Cell><Data ss:Type="String">SF3B4 is decreased in pancreatic cancer and inhibits the growth and migration of cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">Splicing factor 3b subunit 4 acted as a suppressive role in pancreatic cancer and indicated that restoring the function of splicing factor 3b subunit 4 might be a strategy for cancer therapy</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28351319</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">SF3B4</Data></Cell>
    <Cell><Data ss:Type="String">SF3B4 as an early-stage diagnostic marker and driver of hepatocellular carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">SF3B4 indicates early-stage HCC in precancerous lesions, and also functions as an early-stage driver in the development of liver cancer.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29397868</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">SFN</Data></Cell>
    <Cell><Data ss:Type="String">Hypermethylation of 14-3-3 sigma (stratifin) is an early event in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">The 14-3-3 proteins are a family of widely expressed regulatory molecules. Their ability to bind a variety of functionally diverse signaling proteins, including kinases, phosphatases, and transmembrane receptors, allows 14-3-3 proteins to play important roles in a wide range of regulatory processes, such as mitogenic signal transduction, cell cycle control, and apoptotic cell death.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">11423985</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">SFN</Data></Cell>
    <Cell><Data ss:Type="String">Quantitative assessment of promoter hypermethylation during breast cancer development</Data></Cell>
    <Cell><Data ss:Type="String">For RASSF1A and 14-3-3  promoter methylation was demonstrated in epithelial hyperplasia and intraductal papillomas.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">11839581</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">SFN</Data></Cell>
    <Cell><Data ss:Type="String">Unraveling breast cancer heterogeneity through transcriptomic and epigenomic analysis</Data></Cell>
    <Cell><Data ss:Type="String">SFN (stratifin), a TSG involved in cell-cycle control and regulated by TP53, is frequently epigenetically silenced in breast cancer.Similar to RASSF1A, SFN methylation frequently occurs in microdissected atypical hyperplasia and DCIS. SFN methylation, however, has also been scored in physiological breast proliferations and stromal breast tissue, emphasizing the importance of selective tissue sampling when using SFN methylation as a biomarker of breast cancer risk</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19452229</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">SFN</Data></Cell>
    <Cell><Data ss:Type="String">Hypermethylated 14-3-3-sigma and ESR1 gene promoters in serum as candidate biomarkers for the diagnosis and treatment efficacy of breast cancer metastasis</Data></Cell>
    <Cell><Data ss:Type="String">The relationship of 14-3-3-sigma with breast cancer metastasis and progression found in this study suggests a possible application of 14-3-3-sigma as a biomarker to screen for metastasis and to follow up patients treated for metastatic breast cancer, monitoring their disease status and treatment response</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">20487521</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">SFTA1P</Data></Cell>
    <Cell><Data ss:Type="String">Comprehensive characterization of cancer subtype associated long non-coding RNAs and their clinical implications</Data></Cell>
    <Cell><Data ss:Type="String">SFTA1P is identified to be associated with tumor subtypes and their functions as well as the associated proteins are predicted by constructing coding-non-coding co-expression network</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25307233</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">SFTA1P</Data></Cell>
    <Cell><Data ss:Type="String">Co-expression network analysis of long noncoding RNAs (IncRNAs) and cancer genes reveals SFTA1P and CASC2 abnormalities in lung squamous cell carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">SFTA1P and CASC2 were found to be related with most of the oncogenes and tumor supressor gene by co-expression analysis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28118064</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">SFTA1P</Data></Cell>
    <Cell><Data ss:Type="String">The pseudogene-derived long noncoding RNA SFTA1P is down-regulated and suppresses cell migration and invasion in lung adenocarcinoma</Data></Cell>
    <Cell><Data ss:Type="String">SFTA1P is down-regulated and suppresses cell migration and invasion in lung adenocarcinoma</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28231733</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">SFTA1P</Data></Cell>
    <Cell><Data ss:Type="String">Long noncoding RNA SFTA1P promoted apoptosis and increased cisplatin chemosensitivity via regulating the hnRNP-U-GADD45A axis in lung squamous cell carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">SFTA1P promoted apoptosis and increased cisplatin chemosensitivity via regulating the hnRNP-U-GADD45A axis in lung squamous cell </Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29228625</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">SFTA1P</Data></Cell>
    <Cell><Data ss:Type="String">The pseudogene-derived long non-coding RNA SFTA1P suppresses cell proliferation, migration, and invasion in gastric cancer</Data></Cell>
    <Cell><Data ss:Type="String">SFTA1P suppresses cell proliferation, migration, and invasion in gastric cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29523596</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">SNRPA1</Data></Cell>
    <Cell><Data ss:Type="String">Classification and Biomarker Genes Selection for Cancer Gene Expression Data Using Random Forest</Data></Cell>
    <Cell><Data ss:Type="String">The SNCA, USP20, and SNRPA1 genes were selected for prostate cancer with the accuracy of 73.33 and precision of 66.67</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29563929</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">SNRPA1</Data></Cell>
    <Cell><Data ss:Type="String">An oncogenic gene, SNRPA1, regulates PIK3R1, VEGFC, MKI67, CDK1 and other genes in colorectal cancer</Data></Cell>
    <Cell><Data ss:Type="String">These novel findings identified new roles played by SNRPA1 in the progression of CRC and it may become a potential therapeutic target in the treatment of CRC</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31203132</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TAC1</Data></Cell>
    <Cell><Data ss:Type="String">Transformation of breast cells by truncated neurokinin-1 receptor is secondary to activation by preprotachykinin-A peptides</Data></Cell>
    <Cell><Data ss:Type="String">The oncogenic property of Tac1 in breast cells involves concomitant expression of NK1-Tr and vice versa, consequently leading to the production of cytokines with growth promoting functions</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">16291810</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TAC1</Data></Cell>
    <Cell><Data ss:Type="String">Stromal-derived factor-1α induces a non-canonical pathway to activate the endocrine-linked?Tac1?gene in non-tumorigenic breast cells</Data></Cell>
    <Cell><Data ss:Type="String">Tac1 is relevant to breast cancer metastasis, to bone marrow where stromal cells have a significant facilitating function</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">18316470</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TAC1</Data></Cell>
    <Cell><Data ss:Type="String">RE-1-silencing transcription factor shows tumor-suppressor functions and negatively regulates the oncogenic TAC1 in breast cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">REST knockdown in low-metastatic T47D cells and nontumorigenic MCF12A cells resulted in increases in TAC1 induction, proliferation, and migration</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">19246391</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TAC1</Data></Cell>
    <Cell><Data ss:Type="String">Biomarkers for detection and prognosis of breast cancer identified by a functional hypermethylome screen</Data></Cell>
    <Cell><Data ss:Type="String">Methylation of CDO1, CKM, CRIP1, KL and TAC1 correlated with clinical prognostic variables and was a significant prognosticator for poor overall survival in BC patients.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22647880</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TGFBR1</Data></Cell>
    <Cell><Data ss:Type="String">Proteomic Profiling of Exosomes Secreted by Breast Cancer Cells with Varying Metastatic Potential</Data></Cell>
    <Cell><Data ss:Type="String">Presumably aid in targeting the primary cancer cells to specific metastatic sites</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">29115712</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TGFBR1</Data></Cell>
    <Cell><Data ss:Type="String">TGFB1 and TGFBR1 polymorphisms and breast cancer risk in the Nurses' Health Study</Data></Cell>
    <Cell><Data ss:Type="String">No overall associations between the L10P polymorphism of TGFB1 or the TGFBR1 microsatellite were detected. However, we observed an inverse association between the -509 C/T polymorphism of TGFB1 (p-trend = 0.04), which was stronger and more significant among women with estrogen receptor positive breast cancer.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">17848193</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TGFBR1</Data></Cell>
    <Cell><Data ss:Type="String">TGFBR1*6A and Int7G24A variants of transforming growth factor-β receptor 1 in Swedish familial and sporadic breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">TGFBR1*6A variant may be associated with an increased risk of low-risk familial breast cancer and might be a marker for poorly differentiated breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">17848956</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TGFBR1</Data></Cell>
    <Cell><Data ss:Type="String">TGFBR1 signaling and breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">TGFBR1 signaling in breast cancer may have an impact on breast cancer risk assessment and breast cancer prevention</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21461994</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TGFBR1</Data></Cell>
    <Cell><Data ss:Type="String">TGFBR1 polymorphism and risk of breast cancer in Iranian women</Data></Cell>
    <Cell><Data ss:Type="String">The allelic length of TGFBR1 polymorphisms had no significant association with the age at onset or the grade of disease, nor with the expression of progesterone and estrogen receptors and HER2</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26165686</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TGFBR1</Data></Cell>
    <Cell><Data ss:Type="String">Breast Cancer Stem Cells with Tumor- versus Metastasis-Initiating Capacities Are Modulated by TGFBR1 Inhibition</Data></Cell>
    <Cell><Data ss:Type="String">Inhibiting TGFβ signaling shifts the balance toward the former, which may have unanticipated implications for the therapeutic use of TGFβ/TGFBR1 inhibitor</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31257133</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TLR5</Data></Cell>
    <Cell><Data ss:Type="String">Activation of Toll-Like Receptor 5 on Breast Cancer Cells by Flagellin Suppresses Cell Proliferation and Tumor Growth</Data></Cell>
    <Cell><Data ss:Type="String">TLR5 activation by flagellin mediates innate immune response to elicit potent antitumor activity in breast cancer cells themselves, which may serve as a novel therapeutic target for human breast cancer therapy</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21427357</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TLR5</Data></Cell>
    <Cell><Data ss:Type="String">MAP1S Controls Breast Cancer Cell TLR5 Signaling Pathway and Promotes TLR5 Signaling-based Tumor Suppression</Data></Cell>
    <Cell><Data ss:Type="String">Elevated expression of MAP1S in response to flagellin feed-back regulated tumor inflammatory microenvironment in the late stages of TLR5 signaling through degradation of MyD88 in autophagy process</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24466264</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TLR5</Data></Cell>
    <Cell><Data ss:Type="String">TLR5 is a new reporter for triple-negative breast cancer indicated by radioimmunoimaging and fluorescent staining</Data></Cell>
    <Cell><Data ss:Type="String">125 I-antiTLR5 mAb was an ideal agent for non-invasive imaging of TLR5+ tumours; TLR5 may be as a novel molecular target for TNBC non-invasive diagnosis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">31576678</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TLR5</Data></Cell>
    <Cell><Data ss:Type="String">TLR5 is a potential target in vivo monitoring triple-negative breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">TLR5 expressed on triple-negative breast cancer could be a molecular target for monitoring tumor growth in vivo and Flavopiridol may carry out its anti-tumor effect through CDK9-TLR5-NF-κB pathway.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TPP2</Data></Cell>
    <Cell><Data ss:Type="String">Tripeptidyl-peptidase II controls DNA damage responses and in vivo gamma-irradiation resistance of tumors.</Data></Cell>
    <Cell><Data ss:Type="String">TPPII can be targeted for inhibition of tumor therapy resistance.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">17671184</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TPP2</Data></Cell>
    <Cell><Data ss:Type="String">Tripeptidyl-peptidase II controls DNA damage responses and in vivo gamma-irradiation resistance of tumors.</Data></Cell>
    <Cell><Data ss:Type="String">TPPII contains a BRCA COOH-terminal-like motif, contained within sequences of several proteins involved in DNA damage signaling pathways, and this motif was important for nuclear translocation of TPPII and stabilization of p53.TPPII connects signaling by cytosolic/mitochondrial and nuclear PIKK-dependent pathways</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">17671184</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TPP2</Data></Cell>
    <Cell><Data ss:Type="String">Tripeptidyl peptidase II in human oral squamous cell carcinoma.</Data></Cell>
    <Cell><Data ss:Type="String">Overexpression of TPP2 occurs frequently during oral carcinogenesis and might be associated with OSCC progression via SAC activation.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22986808</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TRIOBP</Data></Cell>
    <Cell><Data ss:Type="String">The actin-bundling protein TRIOBP-4 and -5 promotes the motility of pancreatic cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">A novel role of TRIOBP-4/-5 that promotes the motility of pancreatic cancer cells via regulating actin cytoskeleton reorganization in the filopodia of the cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25130170</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TRIOBP</Data></Cell>
    <Cell><Data ss:Type="String">The roles of TRIO and F-actin-binding protein in glioblastoma cells</Data></Cell>
    <Cell><Data ss:Type="String">The present data indicate that TrioBP expression is increased in glioblastoma cell lines and in patients with glioma, suggesting that TrioBP has potential as a diagnostic marker or therapeutic agent for glioma</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29363730</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TRPC5</Data></Cell>
    <Cell><Data ss:Type="String">Increasing circulating exosomes carrying TRPC5 predicts chemoresistance in metastatic breast cancer patients</Data></Cell>
    <Cell><Data ss:Type="String">CirExo-TRPC5 might act as a noninvasive chemoresistance marker and might serve as an adjuvant to the current imaging examination-based chemoresistance</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">BBCE</Data></Cell>
    <Cell><Data ss:Type="Number">28032400</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TRPC5</Data></Cell>
    <Cell><Data ss:Type="String">Transient receptor potential channel TRPC5 is essential for P-glycoprotein induction in drug-resistant cancer cells</Data></Cell>
    <Cell><Data ss:Type="String">In an athymic nude mouse model of adriamycin-resistant human breast tumor, suppressing TRPC5 decreased the growth of tumor xenografts. Nuclear factor of activated T cells isoform c3 (NFATc3) was the transcriptional factor that links the TRPC5 activity to P-gp production</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22988121</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TRPC5</Data></Cell>
    <Cell><Data ss:Type="String">Essential role for TrpC5-containing extracellular vesicles in breast cancer with chemotherapeutic resistance</Data></Cell>
    <Cell><Data ss:Type="String">TrpC5-containing circulating EVs may transfer chemoresistance property to nonchemoresistant recipient cells</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">24733904</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TRPC5</Data></Cell>
    <Cell><Data ss:Type="String">A Methylation-Based Regulatory Network for MicroRNA 320a in Chemoresistant Breast Cancer</Data></Cell>
    <Cell><Data ss:Type="String">MiR-320a is a mediator of chemoresistance by targeting TRPC5 and NFATC3. Expression of miR-320a is regulated by methylation of its promoter and that of ETS-1</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25159093</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TRPC5</Data></Cell>
    <Cell><Data ss:Type="String">TRPC5-induced autophagy promotes drug resistance in breast carcinoma via CaMKKβ/AMPKα/mTOR pathway</Data></Cell>
    <Cell><Data ss:Type="String">A novel role of TRPC5 as an inducer of autophagy, and this suggests a novel mechanism of drug resistance in chemotherapy for breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28600513</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TRPC5</Data></Cell>
    <Cell><Data ss:Type="String">Glycolysis is essential for chemoresistance induced by transient receptor potential channel C5 in colorectal cancer</Data></Cell>
    <Cell><Data ss:Type="String">We demonstrated the essential role of glycolysis in TRPC5 induced chemoresistance in human CRC cells via maintaining [Ca2+]?i?homeostasis</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29463225</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TSC2</Data></Cell>
    <Cell><Data ss:Type="String">Mechanism of Akt1 inhibition of breast cancer cell invasion reveals a protumorigenic role for TSC2</Data></Cell>
    <Cell><Data ss:Type="String">Overexpression of TSC2 rescues the migration phenotype of myr-Akt1-expressing tumor cells, and high levels of TSC2 in breast cancer patients correlate with increased metastasis and reduced survival</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">16537497</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TSC2</Data></Cell>
    <Cell><Data ss:Type="String">ARD1 stabilization of TSC2 suppresses tumorigenesis through the mTOR signaling pathway</Data></Cell>
    <Cell><Data ss:Type="String">ARD1 functions as an inhibitor of the mTOR pathway and that dysregulation of the ARD1-TSC2-mTOR axis may contribute to cancer development</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">20145209</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TSC2</Data></Cell>
    <Cell><Data ss:Type="String">Polymorphic variants in TSC1 and TSC2 and their association with breast cancer phenotypes</Data></Cell>
    <Cell><Data ss:Type="String">TSC1 acts coordinately with TSC2 in a complex to inhibit mTOR, an emerging therapeutic target and known promoter of cell growth and cell cycle progression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">20658316</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TSC2</Data></Cell>
    <Cell><Data ss:Type="String">Loss of Tuberous Sclerosis Complex 2 (TSC2) as a Predictive Biomarker of Response to mTOR Inhibitor Treatment in Patients with Hepatocellular Carcinoma1</Data></Cell>
    <Cell><Data ss:Type="String">Loss of TSC2 may predict improved response to everolimus in HCC patients, but further studies are needed to confirm the predictive role of TSC2 expression for everolimus treatment</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">27751352</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TSC2</Data></Cell>
    <Cell><Data ss:Type="String">ARD1 contributes to IKKβ-mediated breast cancer tumorigenesis</Data></Cell>
    <Cell><Data ss:Type="String">ARD1 prevents mTOR activity and breast cancer cell growth by stabilizing tuberous sclerosis complex 2 (TSC2) to induce autophagy</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30154412</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TSG101</Data></Cell>
    <Cell><Data ss:Type="String">Tumour exosomes inhibit binding of tumour-reactive antibodies to tumour cells and reduce ADCC</Data></Cell>
    <Cell><Data ss:Type="String">Tumour-derived exosomes interfere with the tumour-specific function of immune cells and constitute an additional mechanism how tumours escape from immune surveillance</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">21293856</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TSG101</Data></Cell>
    <Cell><Data ss:Type="String">The breast cancer gene product TSG101: a regulator of ubiquitination?</Data></Cell>
    <Cell><Data ss:Type="String">As the UBC active site residue is replaced in the TSG101 sequence in a similar manner to several other members of the UBC family, we propose a role for TSG101 in regulating the ubiquitination of short-lived gene products</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">9253709</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TSG101</Data></Cell>
    <Cell><Data ss:Type="String">Aberrant splicing of the TSG101 tumor suppressor gene in human breast and ovarian cancers</Data></Cell>
    <Cell><Data ss:Type="String">Truncated TSG101 transcripts that probably represent splice variants are present in some breast and ovarian cancers, but there is no evidence to suggest that loss of this putative tumor suppressor gene plays a role in the molecular pathogenesis of these cancers</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">9773405</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TSG101</Data></Cell>
    <Cell><Data ss:Type="String">Aberrant expression of TSG101 in Taiwan Chinese breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">The aberrant expression of TSG101 in breast cancer is associated with altered cell growth</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">10930114</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TSG101</Data></Cell>
    <Cell><Data ss:Type="String">Down-regulation of TSG101 by small interfering RNA inhibits the proliferation of breast cancer cells through the MAPK/ERK signal pathway</Data></Cell>
    <Cell><Data ss:Type="String">TSG101 may play a biological role through modulation of the MAPK/ERK signaling pathway in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">21117030</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TSG101</Data></Cell>
    <Cell><Data ss:Type="String">A knockout of the Tsg101 gene leads to decreased expression of ErbB receptor tyrosine kinases and induction of autophagy prior to cell death.</Data></Cell>
    <Cell><Data ss:Type="String">Defining particular functions for Tsg101 in processes such as signal transduction and lysosomal/endosomal trafficking</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22479596</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TTTY14</Data></Cell>
    <Cell><Data ss:Type="String">Complex integrated analysis of lncRNAs-miRNAs-mRNAs in oral squamous cell carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">TTTY14 were related with elated with overall survival (OS) and relapse-free survival (RFS)</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28939059</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TTTY14</Data></Cell>
    <Cell><Data ss:Type="String">Comprehensive analysis of a novel four-lncRNA signature as a prognostic biomarker for human gastric cancer</Data></Cell>
    <Cell><Data ss:Type="String">The study indicates that this novel lncRNA expression signature (TTTY14) may be a useful biomarker of the prognosis for GC patients, based on bioinformatics analysis.</Data></Cell>
    <Cell><Data ss:Type="String">biomarker</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">29088841</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TTTY14</Data></Cell>
    <Cell><Data ss:Type="String">Comprehensive analysis of differentially expressed profiles and reconstruction of a competing endogenous RNA network in papillary renal cell carcinoma</Data></Cell>
    <Cell><Data ss:Type="String">This subnetwork consists of hub genes, including lncRNA MEG3, lncRNA Prader-Willi region non-protein coding RNA 1 (PWRN1), hsa-miR-508 and hsa-miR-21, plus certain first neighbors, including neurotrophin 3 (NTF3), tissue inhibitor of metalloproteinase 3 (TIMP3), GRM5-AS1, AP002478.1, TTTY14 and hsa-miR-489.</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30957192</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TYR</Data></Cell>
    <Cell><Data ss:Type="String">Loss of tyrosinase activity confers increased skin tumor susceptibility in mice</Data></Cell>
    <Cell><Data ss:Type="String">In vitro mechanistic studies demonstrated that transfection of the Tyr(Cys) allele in a human squamous cell carcinoma cell line (NCI-H520) increases tyrosinase enzyme activity and confers resistance to hydrogen peroxide-induced oxidative DNA damage</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">15007389</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TYR</Data></Cell>
    <Cell><Data ss:Type="String">MC1R, SLC45A2 and TYR genetic variants involved in melanoma susceptibility in southern European populations: results from a meta-analysis</Data></Cell>
    <Cell><Data ss:Type="String">Adjustment for all clinical potential confounders showed that melanoma risks attributable to MC1R and SLC45A2 variants strongly persisted (OR: 2.01 95% CI: 1.49-2.72 and OR: 0.50, 95% CI: 0.31-0.80, respectively), while the association of TYR p.Arg402Gln was no longer significant</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22464347</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TYR</Data></Cell>
    <Cell><Data ss:Type="String">Tyrosinase as a multifunctional reporter gene for Photoacoustic/MRI/PET triple modality molecular imaging</Data></Cell>
    <Cell><Data ss:Type="String">In vivo PAI/MRI/PET imaging studies showed that MCF-7-TYR tumors achieved significant higher signals and tumor-to-background contrasts than those of MCF-7 tumor. Our study demonstrates that TYR gene can be utilized as a multifunctional reporter gene for PAI/MRI/PET both?in vitro?and?in vivo</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23508226</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">TYR</Data></Cell>
    <Cell><Data ss:Type="String">The tetrapeptide Arg-Leu-Tyr-Glu inhibits VEGF-induced angiogenesis</Data></Cell>
    <Cell><Data ss:Type="String">Arg-Leu-Tyr-Glu (RLYE) effectively inhibited vascular endothelial growth factor (VEGF)-induced endothelial cell proliferation, migration and tube formation, with an IC50 of 0.06-0.08?nM, which was about ten-fold lower than that of the control peptide KLYD (0.79?nM), as well as suppressed developmental angiogenesis in a zebrafish model</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">26051280</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">UCHL1</Data></Cell>
    <Cell><Data ss:Type="String">UCHL1 containing exosomes mediate chemotherapeutic resistance transfer in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">UCH-L1-containing exosomes can transfer chemoresistance to recipient cells and these exosomes may be useful as non-invasive diagnostic biomarkers for detection of chemoresitance in breast cancer patients, achieving more effective and individualized chemotherapy</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">MFBCE</Data></Cell>
    <Cell><Data ss:Type="Number">28334432</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">UCHL1</Data></Cell>
    <Cell><Data ss:Type="String">The Ubiquitin Peptidase UCHL1 Induces G0/G1 Cell Cycle Arrest and Apoptosis Through Stabilizing p53 and Is Frequently Silenced in Breast Cancer</Data></Cell>
    <Cell><Data ss:Type="String">UCHL1 exerts its tumor suppressive functions by inducing G0/G1cell cycle arrest and apoptosis in breast tumorigenesis, requiring its deubiquitinase activity. Its frequent silencing by promoter CpG methylation may serve as a potential tumor marker for breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">22279545</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">UCHL1</Data></Cell>
    <Cell><Data ss:Type="String">Differential expression of ubiquitin carboxy-terminal hydrolase L1 in breast carcinoma and its biological significance</Data></Cell>
    <Cell><Data ss:Type="String">The high expression of UCHL1 in metaplastic carcinomas of the breast, which is pathogenically related to epithelial-mesenchymal transition, may implicate an association between UCHL1 expression and the epithelial-mesenchymal transition in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">23664488</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">UCHL1</Data></Cell>
    <Cell><Data ss:Type="String">UCHL1 provides diagnostic and antimetastatic strategies due to its deubiquitinating effect on HIF-1α</Data></Cell>
    <Cell><Data ss:Type="String">UCHL1 promotes metastases as a deubiquitinating enzyme for HIF-1α, which justifies exploiting it as a prognostic marker and therapeutic target of cancers</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">25615526</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">UCHL1</Data></Cell>
    <Cell><Data ss:Type="String">UCH-L1 promotes invasion of breast cancer cells through activating Akt signaling pathway</Data></Cell>
    <Cell><Data ss:Type="String">UCH-L1 promotes invasion of breast cancer cells and might serve as a potential therapeutic target for treatment of human patients with breast cancers</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28636190</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">UCHL1</Data></Cell>
    <Cell><Data ss:Type="String">UCHL1-HIF-1 axis-mediated antioxidant property of cancer cells as a therapeutic target for radiosensitization</Data></Cell>
    <Cell><Data ss:Type="String">Cancer cells acquire antioxidant and radioresistant phenotypes through UCHL1-HIF-1-mediated metabolic reprogramming including the activation of PPP and provide a rational basis for targeting this gene network for radiosensitization</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">28761052</Data></Cell>
   </Row>
   <Row>
    <Cell><Data ss:Type="String">USF1</Data></Cell>
    <Cell><Data ss:Type="String">The pro-metastasis effect of circANKS1B in breast cancer</Data></Cell>
    <Cell><Data ss:Type="String">USF1 transcriptionally elevated ESRP1 and TGF-β1 expression through directly binding to their promoters, thereby activating TGF-β1 signaling to enhance EMT and metastasis-SF1 enhances breast cancer invasion and metastasis by transcriptionally elevating TGF-β1 expression</Data></Cell>
    <Cell><Data ss:Type="String">molecular function</Data></Cell>
    <Cell><Data ss:Type="String">CBC</Data></Cell>
    <Cell><Data ss:Type="Number">30454010</Data></Cell>
   </Row>
  </Table>
  <WorksheetOptions xmlns="urn:schemas-microsoft-com:office:excel">
   <PageSetup>
    <Header x:Margin="0.3"/>
    <Footer x:Margin="0.3"/>
    <PageMargins x:Bottom="0.75" x:Left="0.7" x:Right="0.7" x:Top="0.75"/>
   </PageSetup>
   <Selected/>
   <Panes>
    <Pane>
     <Number>3</Number>
     <RangeSelection>R1C1:R1107C6</RangeSelection>
    </Pane>
   </Panes>
   <ProtectObjects>False</ProtectObjects>
   <ProtectScenarios>False</ProtectScenarios>
  </WorksheetOptions>
 </Worksheet>
</Workbook>
