| Summary: | Yanhua Yu,1 Fang Yu,1 Pijiang Sun2 1Department of Dermatology, Weihai Central Hospital Affiliated to Qingdao University, Weihai 264400, People’s Republic of China; 2Department of Hepatobiliary and Abdominal Hernias Surgery, Weihai Central Hospital Affiliated to Qingdao University, Weihai 264400, People’s Republic of ChinaCorrespondence: Pijiang SunDepartment of Hepatobiliary and Abdominal Hernias Surgery, Weihai Central Hospital Affiliated to Qingdao University, No. 3 Mishandong Road, Wendeng District, Weihai 264400, Shandong, People’s Republic of ChinaTel +86 152 6441 0981Email beciham@163.comIntroduction: Recently, the incidence of melanoma has been rising and there is a lack of effective targeted therapies. The regulatory mechanisms of microRNA-1246 (miR-1246) have been found in many cancers, except melanoma. This study focused on the regulatory mechanism of miR-1246 in melanoma development.Methods: The expression of miR-1246 was assessed using quantitative real-time polymerase chain reaction (RT-qPCR). Cell viability and metastasis were detected by Transwell and MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assays. The protein expression of epithelial mesenchymal transition (EMT) makers was assessed by Western blot analysis. The target gene of miR-1246 was detected using luciferase reporter assay.Results: MiR-1246 expression was increased in melanoma tissues and cells. In addition, upregulation of miR-1246 promoted cell viability and metastasis in melanoma. Forkhead box protein A2 (FOXA2) was confirmed to be a direct target of miR-1246. And FOXA2 expression was decreased in melanoma and was suppressed by miR-1246. Importantly, upregulation of FOXA2 restored the carcinogenesis of miR-1246 in melanoma.Conclusion: MiR-1246 promoted cell viability and metastasis in melanoma by inhibiting FOXA2 expression.Keywords: miR-1246, melanoma, cell viability, cell metastasis, FOXA2
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