{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T04:20:16Z","timestamp":1790223616873,"version":"4.1.0"},"reference-count":32,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2020,3,24]],"date-time":"2020-03-24T00:00:00Z","timestamp":1585008000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["febs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["FEBS Open Bio"],"published-print":{"date-parts":[[2020,5]]},"abstract":"<jats:p>Human melanoma is a highly malignant tumor originating from cutaneous melanocytes. The noncoding RNA microRNA (miR)\u201021\u20105p has been reported to be expressed at high levels in malignant melanocytic skin tissues, but its potential functional role in melanoma remains poorly understood. Here, we explored the cellular effects of miR\u201021\u20105p on melanoma <jats:italic>in\u00a0vitro<\/jats:italic> and the underlying mechanisms. Quantitative real\u2010time PCR was used to show that miR\u201021\u20105p is significantly up\u2010regulated in clinical samples from patients with melanoma as compared with adjacent noncancerous tissues. Overexpression of miR\u201021\u20105p significantly enhanced, whereas knockdown attenuated, cell proliferation and G1\/S transition in melanoma cell lines (A375 and M14). Luciferase reporter assays were used to show that the cyclin\u2010dependent kinase inhibitor 2C (<jats:italic>CDKN2C<\/jats:italic>) is a downstream target of miR\u201021\u20105p. Furthermore, miR\u201021\u20105p mimics resulted in a decrease in CDKN2C expression, and <jats:italic>CDKN2C<\/jats:italic> expression was observed to be inversely correlated with miR\u201021\u20105p expression in melanoma tissues. Rescue experiments were performed to show that overexpression of <jats:italic>CDKN2C<\/jats:italic> partially reversed the effects of miR\u201021\u20105p up\u2010regulation on A375 cells. Consistently, knockdown of CDKN2C abolished the effects of miR\u201021\u20105p down\u2010regulation on A375 cells. Overall, our studies demonstrate that miR\u201021\u20105p can promote the growth of melanoma cells by targeting <jats:italic>CDKN2C<\/jats:italic>, which may induce G0\/G1 phase arrest of melanoma cells.<\/jats:p>","DOI":"10.1002\/2211-5463.12819","type":"journal-article","created":{"date-parts":[[2020,2,24]],"date-time":"2020-02-24T07:51:25Z","timestamp":1582530685000},"page":"752-760","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":31,"title":["miR\u201021\u20105p promotes cell proliferation and G1\/S transition in melanoma by targeting CDKN2C"],"prefix":"10.1002","volume":"10","author":[{"given":"Zhaohui","family":"Yang","sequence":"first","affiliation":[{"name":"Department of Burns and Plastic Surgery Affiliated Hospital of North Sichuan Medical College Nanchong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bo","family":"Liao","sequence":"additional","affiliation":[{"name":"Department of Urology 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