Renal cell cancer(RCC)remains one of the most lethal types of cancer in adults.Micro RNAs(mi RNAs)play key roles in the pathogenesis of RCC.The role of mi R-206 in RCC has not been fully understood.The purpose of this...Renal cell cancer(RCC)remains one of the most lethal types of cancer in adults.Micro RNAs(mi RNAs)play key roles in the pathogenesis of RCC.The role of mi R-206 in RCC has not been fully understood.The purpose of this study was to examine the role of mi R-206 in the regulation of proliferation and metastasis of RCC and the possible mechanism.mi R-206 expression was detected by reverse transcription?quantitative polymerase chain reaction(RT-q PCR)in RCC cell lines(786-O and OS-RC-2 cells)and clinical samples.MTS[3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium]method,colony formation and transwell assay were used to detect the tumor-suppressing ability of mi R-206 in RCC.Luciferase assay was performed to verify the precise target of mi R-206.The results showed that the expression of mi R-206 was significantly down-regulated in RCC tissues and cells.The expression level of cyclin G-associated kinase(GAK),a master regulator of tumor proliferation and metastasis,was up-regulated with the decrease in mi R-206 in RCC tissues as well as RCC cell lines.In addition,the mi R-206 inhibitor promoted the proliferation,migration and invasion of 786-O and OS-RC-2 cells.Bioinformatics combined with luciferase and Western blot assays revealed that mi R-206 inhibited the expression of GAK.Moreover,mi R-206 regulates RCC cell growth partly through targeting GAK.Our study indicated that mi R-206 functions as a tumor suppressor in regulating the proliferation,migration and invasion of RCC by directly targeting GAK,and it holds promises as a potential therapeutic target for RCC.展开更多
文摘Renal cell cancer(RCC)remains one of the most lethal types of cancer in adults.Micro RNAs(mi RNAs)play key roles in the pathogenesis of RCC.The role of mi R-206 in RCC has not been fully understood.The purpose of this study was to examine the role of mi R-206 in the regulation of proliferation and metastasis of RCC and the possible mechanism.mi R-206 expression was detected by reverse transcription?quantitative polymerase chain reaction(RT-q PCR)in RCC cell lines(786-O and OS-RC-2 cells)and clinical samples.MTS[3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium]method,colony formation and transwell assay were used to detect the tumor-suppressing ability of mi R-206 in RCC.Luciferase assay was performed to verify the precise target of mi R-206.The results showed that the expression of mi R-206 was significantly down-regulated in RCC tissues and cells.The expression level of cyclin G-associated kinase(GAK),a master regulator of tumor proliferation and metastasis,was up-regulated with the decrease in mi R-206 in RCC tissues as well as RCC cell lines.In addition,the mi R-206 inhibitor promoted the proliferation,migration and invasion of 786-O and OS-RC-2 cells.Bioinformatics combined with luciferase and Western blot assays revealed that mi R-206 inhibited the expression of GAK.Moreover,mi R-206 regulates RCC cell growth partly through targeting GAK.Our study indicated that mi R-206 functions as a tumor suppressor in regulating the proliferation,migration and invasion of RCC by directly targeting GAK,and it holds promises as a potential therapeutic target for RCC.
