MiR-144 inhibits cell proliferation of renal cell carcinoma by targeting MTOR.
10.1007/s11596-016-1564-0
- Author:
Cheng XIANG
1
;
Shi-peng CUI
2
;
You KE
3
Author Information
1. Department of General Surgery, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310009, China.
2. Department of General Surgery, the First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
3. Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. youke@hust.edu.cn.
- Publication Type:Journal Article
- Keywords:
mTOR;
miR-144;
proliferation;
renal cell carcinoma (RCC)
- MeSH:
Carcinoma, Renal Cell;
genetics;
metabolism;
pathology;
Case-Control Studies;
Cell Line, Tumor;
Cell Proliferation;
Female;
G2 Phase;
Humans;
Kidney Neoplasms;
genetics;
metabolism;
pathology;
Male;
MicroRNAs;
genetics;
metabolism;
Middle Aged;
S Phase;
TOR Serine-Threonine Kinases;
genetics;
metabolism
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2016;36(2):186-192
- CountryChina
- Language:English
-
Abstract:
MicroRNAs (miRNAs) modulate the expression of tumorigenesis-related genes and play important roles in the development of various types of cancers. It has been reported that miR-144 is dysregulated and involved in multiple malignant tumors, but its role in renal cell carcinoma (RCC) remains elusive. In this study, we demonstrated miR-144 was significantly downregulated in human RCC. The decreased miR-144 correlated with tumor size and TNM stage. Moreover, overexpression of miR-144 in vitro suppressed RCC cell proliferation and G2 transition, which were reversed by inhibition of miR-144. Bioinformatic analysis predicted that mTOR was a potential target of miR-144, which was further confirmed by dual luciferase reporter assay. Additionally, the examination of clinical RCC specimens revealed that miR-144 was inversely related to mTOR. Furthermore, knocking down mTOR with siRNA had the same biological effects as those of miR-144 overexpression in RCC cells, including cell proliferation inhibition and S/G2 cell cycle arrest. In conclusion, our results indicate that miR-144 affects RCC progression by inhibiting mTOR expression, and targeting miR-144 may act as a novel strategy for RCC treatment.
