MiR-186 represses progression of renal cell cancer by directly targeting CDK6

The function of miR-186 in the progression of renal cell carcinoma (RCC) remains poorly investigated. Our study aims to identify the molecular mechanism underlying miR-186-regulated proliferation, migration and invasion of RCC. Firstly, our data confirmed that miR-186 was significantly reduced and CDK6 was obviously increased in RCC tissues and cells. MiR-186 or CDK6 was associated with advanced TNM stage, lymph node metastasis and poor prognosis. MiR-186 significantly inhibited cell proliferation, migration, invasion and in vivo tumor growth, induced apoptosis, and blocked cell cycle progression in G0/G1 phase. MiR-186 also induced Bax expression and inhibited the expressions of Bcl-2, cyclin D1 and epithelial-mesenchymal transition (EMT)-related genes. Additionally, CDK6 expression was downregulated by miR-186 via binding to its 3MODIFIER LETTER PRIME-untranslated region (3MODIFIER LETTER PRIME-UTR). Moreover, ectopic expression of CDK6 could partially abrogate the inhibitory effect of miR-186. In conclusion, miR-186 suppresses proliferation, migration and invasion of RCC by inhibiting CDK6 expression.