Micro RNAs（mi RNAs） modulate the expression of tumorigenesis-related genes and play important roles in the development of various types of cancers. It has been reported that mi R-144 is dysregulated and involved in ...Micro RNAs（mi RNAs） modulate the expression of tumorigenesis-related genes and play important roles in the development of various types of cancers. It has been reported that mi R-144 is dysregulated and involved in multiple malignant tumors, but its role in renal cell carcinoma（RCC） remains elusive. In this study, we demonstrated mi R-144 was significantly downregulated in human RCC. The decreased mi R-144 correlated with tumor size and TNM stage. Moreover, overexpression of mi R-144 in vitro suppressed RCC cell proliferation and G2 transition, which were reversed by inhibition of mi R-144. Bioinformatic analysis predicted that m TOR was a potential target of mi R-144, which was further confirmed by dual luciferase reporter assay. Additionally, the examination of clinical RCC specimens revealed that mi R-144 was inversely related to m TOR. Furthermore, knocking down m TOR with si RNA had the same biological effects as those of mi R-144 overexpression in RCC cells, including cell proliferation inhibition and S/G2 cell cycle arrest. In conclusion, our results indicate that mi R-144 affects RCC progression by inhibiting m TOR expression, and targeting mi R-144 may act as a novel strategy for RCC treatment.展开更多
文摘Micro RNAs（mi RNAs） modulate the expression of tumorigenesis-related genes and play important roles in the development of various types of cancers. It has been reported that mi R-144 is dysregulated and involved in multiple malignant tumors, but its role in renal cell carcinoma（RCC） remains elusive. In this study, we demonstrated mi R-144 was significantly downregulated in human RCC. The decreased mi R-144 correlated with tumor size and TNM stage. Moreover, overexpression of mi R-144 in vitro suppressed RCC cell proliferation and G2 transition, which were reversed by inhibition of mi R-144. Bioinformatic analysis predicted that m TOR was a potential target of mi R-144, which was further confirmed by dual luciferase reporter assay. Additionally, the examination of clinical RCC specimens revealed that mi R-144 was inversely related to m TOR. Furthermore, knocking down m TOR with si RNA had the same biological effects as those of mi R-144 overexpression in RCC cells, including cell proliferation inhibition and S/G2 cell cycle arrest. In conclusion, our results indicate that mi R-144 affects RCC progression by inhibiting m TOR expression, and targeting mi R-144 may act as a novel strategy for RCC treatment.
