MiR-144 Inhibits Cell Proliferation of Renal Cell Carcinoma by Targeting MTOR

• Published in: Journal of Huazhong University of Science and Technology. Medical sciences Vol. 36; no. 2; pp. 186 - 192
• Main Author: 项承 崔世鹏 柯悠
• Format: Journal Article
• Language: English
• Published: Wuhan Huazhong University of Science and Technology 01.04.2016; Department of General Surgery, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China%Department of General Surgery, the First Affiliated Hospital of Soochow University, Suzhou 215006, China%Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China
• Subjects: Carcinoma, Renal Cell - genetics; Carcinoma, Renal Cell - metabolism; Carcinoma, Renal Cell - pathology; Case-Control Studies; Cell Line, Tumor; Cell Proliferation; Female; G2 Phase; Humans; Kidney Neoplasms - genetics; Kidney Neoplasms - metabolism; Kidney Neoplasms - pathology; Male; Medicine; Medicine & Public Health; MicroRNAs - genetics; MicroRNAs - metabolism; Middle Aged; mTOR; S Phase; TOR Serine-Threonine Kinases - genetics; TOR Serine-Threonine Kinases - metabolism; 微RNA; 恶性肿瘤; 癌细胞; 碾压混凝土; 细胞周期阻滞; 细胞增殖; 肾细胞; mTOR; proliferation; miR-144; renal cell carcinoma (RCC)
• ISSN: 1672-0733; 1993-1352
• DOI: 10.1007/s11596-016-1564-0

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.