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.

中文翻译：

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MiR-206通过抑制CDK6表达来抑制肾细胞癌的增殖和上皮间质转化。

越来越多的证据表明，miRNA参与人肾细胞癌（RCC）的肿瘤发生。但是，miR-206的作用仍然未知。这项研究旨在研究miR-206在RCC进展中的可能机制。在此，与邻近的正常肾组织和HK-2细胞相比，在RCC组织和细胞系中miR-206水平显着降低，而CDK6水平明显升高。MiR-206与淋巴结转移和TNM分期呈负相关，并且是RCC中独立的预后因素。MiR-206有效引起细胞凋亡和细胞周期停滞在G0 / G1期，并影响裸鼠异种移植瘤的生长。MiR-206还通过调节EMT相关基因的表达来抑制RCC细胞的迁移和侵袭。双荧光素酶测定法证明CDK6是miR-206的直接靶标。CDK6沉默加剧了miR-206的抑制作用。总之，miR-206通过抑制CDK6表达来抑制RCC的增殖和EMT。miR-206 / CDK6轴可能为RCC的肿瘤发生提供新的见解。