Lihua Guo1, Dayu Wang, Zhiping Zhang. 1. Department of Nephrology, China-Japan Union Hospital of Jilin University, Changchun, Jilin Province, P.R. China.
Abstract
PURPOSE: Clear cell renal cell carcinoma (ccRCC) accounts for 70-80% of renal cell carcinomas. Various microRNAs (miRs) have been reported to affect the tumorigenesis of ccRCC. However, the role of miR-384 in ccRCC is still unknown. Thus, the purpose of this study was to investigate the function of miR-384 in ccRCC. METHODS: qRT-PCR or Western blot were employed to examine the expressions of miR-384 and CDK6 in ccRCC tissues or cell lines. MTT and transwell assays were applied to measure cell proliferation and motility. The survival rate was analyzed by Kaplan-Meier method accompanied with log-rank test. Dual luciferase assay was used to verify the relationship among miR-384 and CDK6 in ccRCC cells. RESULTS: MiR-384 was downregulated in ccRCC tissues and cell lines, and its overexpression inhibited cell proliferation and motility in ccRCC. In addition, miR-384 was found to be a marker for good prognosis in ccRCC. Furthermore, CDK6 was confirmed to be directly targeted by miR-384, and upregulation of CDK6 restored the inhibitory effects of miR- 384 in ccRCC. CONCLUSION: MiR-384 repressed tumorigenesis by regulating CDK6 in ccRCC and predicted good prognosis for ccRCC.
PURPOSE:Clear cell renal cell carcinoma (ccRCC) accounts for 70-80% of renal cell carcinomas. Various microRNAs (miRs) have been reported to affect the tumorigenesis of ccRCC. However, the role of miR-384 in ccRCC is still unknown. Thus, the purpose of this study was to investigate the function of miR-384 in ccRCC. METHODS: qRT-PCR or Western blot were employed to examine the expressions of miR-384 and CDK6 in ccRCC tissues or cell lines. MTT and transwell assays were applied to measure cell proliferation and motility. The survival rate was analyzed by Kaplan-Meier method accompanied with log-rank test. Dual luciferase assay was used to verify the relationship among miR-384 and CDK6 in ccRCC cells. RESULTS:MiR-384 was downregulated in ccRCC tissues and cell lines, and its overexpression inhibited cell proliferation and motility in ccRCC. In addition, miR-384 was found to be a marker for good prognosis in ccRCC. Furthermore, CDK6 was confirmed to be directly targeted by miR-384, and upregulation of CDK6 restored the inhibitory effects of miR- 384 in ccRCC. CONCLUSION:MiR-384 repressed tumorigenesis by regulating CDK6 in ccRCC and predicted good prognosis for ccRCC.