{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,5,14]],"date-time":"2025-05-14T01:48:47Z","timestamp":1747187327563,"version":"3.40.5"},"reference-count":34,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2021,3,19]],"date-time":"2021-03-19T00:00:00Z","timestamp":1616112000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Oral Diseases"],"published-print":{"date-parts":[[2022,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>To explore the effect of miR\u2010873\u20105p on proliferation, apoptosis, migration, and invasion of tongue squamous cell carcinoma (TSCC) by targeting <jats:italic>SEC11A<\/jats:italic>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Tongue squamous cell carcinoma tissues were collected and performed by qRT\u2010PCR and Western blotting to determine the expression of miR\u2010873\u20105p and SPC18. SCC9 and CAL\u201027 cells were transfected and divided into Mock, mimic NC, miR\u2010873\u20105p mimic, SEC11A, and miR\u2010873\u20105p mimic\u00a0+\u00a0SEC11A groups. Then, a series of experiments including cell count kit 8 (CCK\u20108), wound healing, Transwell, and flow cytometry were conducted. Besides, Western blotting was used to detect the expression of SPC18 and EGFR pathway\u2010related proteins.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>MiR\u2010873\u20105p was downregulated while SPC18 was upregulated in TSCC, and miR\u2010873\u20105p was negatively correlated with SPC18. Dual luciferase reporter gene assay confirmed <jats:italic>SEC11A<\/jats:italic> to be a target of miR\u2010873\u20105p. Cell proliferation, migration, and invasion of SCC9 and CAL\u201027 cells in miR\u2010873\u20105p mimic group were decreased with increased cell apoptosis, presenting with downregulations of SPC18 and EGFR pathway\u2010related proteins, while cells in SEC11A group manifested totally different changes. Moreover, the inhibitory effect of miR\u2010873\u20105p mimic on TSCC cell growth was abolished by <jats:italic>SEC11A<\/jats:italic> overexpression.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Overexpression of miR\u2010873\u20105p may suppress cell proliferation, migration, and invasion, but facilitate apoptosis in TSCC via targeting <jats:italic>SEC11A<\/jats:italic>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/odi.13830","type":"journal-article","created":{"date-parts":[[2021,3,6]],"date-time":"2021-03-06T08:30:15Z","timestamp":1615019415000},"page":"1509-1518","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["MiR\u2010873\u20105p modulates progression of tongue squamous cell carcinoma via targeting <i>SEC11A<\/i>"],"prefix":"10.1111","volume":"28","author":[{"given":"Yao","family":"Yao","sequence":"first","affiliation":[{"name":"Department of Stomatology Jingzhou Central Hospital The Second Clinical Medical College Yangtze University  Jingzhou China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiao\u2010Qin","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Stomatology Jingzhou Central Hospital The Second Clinical Medical College Yangtze University  Jingzhou China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Feng\u2010Ying","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Stomatology Dongfang Hospital Beijing University of Chinese Medicine  Beijing China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0488-7337","authenticated-orcid":false,"given":"Jing\u2010Wen","family":"Mu","sequence":"additional","affiliation":[{"name":"Department of Stomatology Dongfang Hospital Beijing University of Chinese Medicine  Beijing 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