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 3ʹ-untranslated region (3ʹ-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.

中文翻译：

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MiR-186通过直接靶向CDK6抑制肾细胞癌的进展。

关于miR-186在肾细胞癌（RCC）进程中的功能的研究仍很少。我们的研究旨在确定miR-186调控RCC增殖，迁移和侵袭的分子机制。首先，我们的数据证实，在RCC组织和细胞中miR-186显着减少，而CDK6明显增加。MiR-186或CDK6与晚期TNM分期，淋巴结转移和不良预后有关。MiR-186显着抑制细胞增殖，迁移，侵袭和体内肿瘤生长，诱导细胞凋亡，并阻止G0 / G1期的细胞周期进程。MiR-186还诱导Bax表达并抑制Bcl-2，细胞周期蛋白D1和上皮-间质转化（EMT）相关基因的表达。另外，miK-186通过结合其3′-非翻译区（3′-UTR）而下调CDK6的表达。此外，CDK6的异位表达可以部分消除miR-186的抑制作用。总之，miR-186通过抑制CDK6表达来抑制RCC的增殖，迁移和侵袭。