MiR-206 suppresses proliferation and epithelial-mesenchymal transition of renal cell carcinoma by inhibiting CDK6 expression

Abstract

Increasing evidence indicates that miRNAs are involved in tumorigenesis of human renal cell carcinoma (RCC). However, the role of miR-206 is still unknown. This study aimed to investigate the possible mechanism of miR-206 in progression of RCC. Here, compared with adjacent normal renal tissues and HK-2 cells, miR-206 level was markedly decreased, whereas CDK6 level was obviously increased in RCC tissues and cell lines. MiR-206 was inversely associated with lymph node metastasis and TNM stage, and acted as an independent prognostic factor in RCC. MiR-206 effectively caused apoptosis and cell cycle arrest at G0/G1 phase, and affected the growth of xenograft tumor of nude mice. MiR-206 also inhibited migration and invasion of RCC cells by modulating the expressions of EMT-related genes. Dual-luciferase assay demonstrated CDK6 was a direct target of miR-206. CDK6 silencing aggravated the inhibition effects of miR-206. In conclusion, miR-206 suppresses proliferation and EMT of RCC by inhibiting CDK6 expression. The miR-206/CDK6 axis may provide a novel insight into tumorigenesis of RCC.