{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,11]],"date-time":"2026-10-11T13:29:40Z","timestamp":1791725380373,"version":"4.3.4"},"reference-count":35,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2014,9,29]],"date-time":"2014-09-29T00:00:00Z","timestamp":1411948800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/3.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cancer Science"],"published-print":{"date-parts":[[2014,10]]},"abstract":"<jats:p>Epithelial\u2010to\u2010mesenchymal transition (<jats:styled-content style=\"fixed-case\">EMT<\/jats:styled-content>) is implicated in embryonic development and various pathological events. Transforming growth factor beta (TGF\u03b2) has been reported to induce <jats:styled-content style=\"fixed-case\">EMT<\/jats:styled-content> in tumor cells, which is a critical step in the process of metastasis leading to cancer spreading and treatment failure. However, the involvement of micro<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> during the <jats:styled-content style=\"fixed-case\">EMT<\/jats:styled-content> process in tongue squamous cell carcinoma (<jats:styled-content style=\"fixed-case\">TSCC<\/jats:styled-content>) remains to be determined. To address this question, <jats:styled-content style=\"fixed-case\">TSCC<\/jats:styled-content> cell lines <jats:styled-content style=\"fixed-case\">SCC<\/jats:styled-content>9 and <jats:styled-content style=\"fixed-case\">CAL<\/jats:styled-content>27 were treated with human recombinant TGF\u03b21 for 48\u00a0h. mi<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> microarray illustrated that miR\u2010639 was significantly downregulated in <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u03b2\u2010treated <jats:styled-content style=\"fixed-case\">SCC<\/jats:styled-content>9 cells. Ectopic expression of miR\u2010639 with mi<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> mimics effectively blocked <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u03b2\u2010induced <jats:styled-content style=\"fixed-case\">EMT<\/jats:styled-content> in <jats:styled-content style=\"fixed-case\">SCC<\/jats:styled-content>9 and <jats:styled-content style=\"fixed-case\">CAL<\/jats:styled-content>27 cells, but inhibition of miR\u2010639 in <jats:styled-content style=\"fixed-case\">SCC<\/jats:styled-content>9 and <jats:styled-content style=\"fixed-case\">CAL<\/jats:styled-content>27 cells with antisense oligonucleotides induced <jats:styled-content style=\"fixed-case\">EMT<\/jats:styled-content>. Computational micro<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> target predictions detected a conserved sequence matching to the seed region of miR\u2010639 in the 3\u2032\u2010<jats:styled-content style=\"fixed-case\">UTR<\/jats:styled-content> of <jats:italic><jats:styled-content style=\"fixed-case\">FOXC<\/jats:styled-content>1<\/jats:italic> m<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>. Luciferase reporter assays revealed that miR\u2010639 targets <jats:italic><jats:styled-content style=\"fixed-case\">FOXC<\/jats:styled-content>1<\/jats:italic>. Ectopic expression of <jats:styled-content style=\"fixed-case\">FOXC<\/jats:styled-content>1 induces <jats:styled-content style=\"fixed-case\">EMT<\/jats:styled-content> in <jats:styled-content style=\"fixed-case\">TSCC<\/jats:styled-content> cells. Silencing <jats:styled-content style=\"fixed-case\">FOXC<\/jats:styled-content>1 expression blocked <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u03b2\u2010induced <jats:styled-content style=\"fixed-case\">EMT<\/jats:styled-content> in <jats:styled-content style=\"fixed-case\">SCC<\/jats:styled-content>9 cells. Clinically, reduced miR\u2010639 expression was associated with metastasis in <jats:styled-content style=\"fixed-case\">TSCC<\/jats:styled-content> and poor patient survival. The data from the present study suggest that reduced expression of miR\u2010639 underscores the mechanism of <jats:styled-content style=\"fixed-case\">TGF<\/jats:styled-content>\u03b2\u2010induced <jats:styled-content style=\"fixed-case\">EMT<\/jats:styled-content> in <jats:styled-content style=\"fixed-case\">TSCC<\/jats:styled-content> by targeting <jats:italic><jats:styled-content style=\"fixed-case\">FOXC<\/jats:styled-content>1<\/jats:italic> and may serve as therapeutic targets in the process of metastasis.<\/jats:p>","DOI":"10.1111\/cas.12499","type":"journal-article","created":{"date-parts":[[2014,8,13]],"date-time":"2014-08-13T14:41:31Z","timestamp":1407940891000},"page":"1288-1298","source":"Crossref","is-referenced-by-count":63,"title":["miR\u2010639 regulates transforming growth factor beta\u2010induced epithelial\u2013mesenchymal transition in human tongue cancer cells by targeting 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