miR-182 promotes cell proliferation and invasion by inhibiting APC in melanoma

Objective: Common treatment methods have shown a lack of therapeutic effect in melanoma, a type of malignant tumor. The pathogenesis of melanoma is not yet fully clear, therefore, search for a new treatment strategy is urgent. Recent studies have demonstrated that miR-182 is remarkably over-expressed in human melanoma. Our study aimed to explore the underlying mechanism of miR-182 on melanoma. Methods: In this study, the expression level of miR-182 was detected using RT-PCR in melanoma and adjacent tissues as well as in HEM-m, A375, A2058, and WM35 cell lines. Functions of miR-182 were investigated by using CCK-8 on cell proliferation, apoptosis, invasion, and cell cycle on A375 cells. Moreover, expression levels of Frz, Dsh, beta-catenin, APC, Axin, GSK-3 beta, and CK1 were detected by Western blotting after knockdown and overexpression of miR-182. Overexpression of miR-182 and knockdown of APC was used to demonstrate regulated functions in melanoma. Results: Expression levels of miR-182 were significantly upregulated in melanoma tissues and cell lines. Overexpression of miR-182 promoted cell proliferation, migration, and invasion while inhibiting cell apoptosis and cell cycle in S phase. Overexpression of miR-182 upregulated expression levels of beta-catenin and APC. Overexpression of miR-182 and knockdown of APC inhibited proliferation of melanoma cells and tumors. Conclusion: Overexpression of miR-182 promotes cell proliferation and invasion by targeting to APC in melanoma. The pathogenesis of miR-182 and APC might provide therapeutic targets for treatment of melanoma in the molecular level.