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MicroRNA-133a-5p inhibiting metastatic capacity of renal clear cell carcinoma through regulating MON2.

OBJECTIVE
We aimed at analyzing the correlation between microRNA-133a-5p expression and clinical pathological parameters in patients with clear cell renal cell carcinoma (ccRCC) and exploring the mechanism by which microRNA-133a-5p affects the biological behavior of ccRCC cells.


PATIENTS AND METHODS
MicroRNA-133a-5p expression in ccRCC tissues and cell lines were examined by quantitative real-time polymerase chain reaction (qRT-PCR), and the relationship between ATG14 expression and clinicopathological parameters of ccRCC patients was analyzed. A control group (NC mimic) and a microRNA-133a-5p overexpression group (microRNA-133a-5p mimic) were set in the ccRCC cell lines ACHN and 786-O, respectively. The impacts of microRNA-133a-5p on the proliferation and invasion of ccRCC cells were evaluated through performing Cell Counting Kit-8 (CCK-8) and transwell tests, respectively. We further explored the interaction between microRNA-133a-5p and its downstream target gene WNK2 by bioinformatics analysis and Luciferase assay.


RESULTS
Both in ccRCC tissues and cell lines, microRNA-133a-5p showed a significantly reduced expression, which could be used to predict poor prognosis of ccRCC patients. Upregulation of microRNA-133a-5p markedly blunted the proliferation and migratory capacities of HCC cells. Bioinformatics analysis suggested that microRNA-133a-5p can target MON2. In addition, qPCR assay indicated an increased expression of MON2 in ccRCC cell lines and tissues, which was negatively correlated with microRNA-133a-5p. Finally, in vitro cell reverse experiments suggested that overexpression of MON2 counteracted the inhibitory effects of overexpression of microRNA-133a-5p on the proliferation and metastatic capacity of ccRCC.


CONCLUSIONS
This study suggests that the reduced expression of microRNA-133a-5p in ccRCC tissue specimens can predict poor prognosis of ccRCC patients. At the same time, microRNA-133a-5p may suppress the proliferation capacity and metastasis of ccRCC cells by acting on MON2.