miR-206 inhibits renal cell cancer growth by targeting GAK.
- Author:
Chao WEI
1
;
Shen WANG
1
;
Zhang-Qun YE
1
;
Zhi-Qiang CHEN
2
Author Information
1. Department of Urology, Huazhong University of Science and Technology, Wuhan, 430030, China.
2. Department of Urology, Huazhong University of Science and Technology, Wuhan, 430030, China. 115630522@qq.com.
- Publication Type:Journal Article
- Keywords:
G-associated kinase;
miR-206;
renal cell cancer
- MeSH:
Adult;
Aged;
Carcinoma, Renal Cell;
genetics;
metabolism;
pathology;
Cell Line, Tumor;
Cell Movement;
Cell Proliferation;
Female;
Gene Expression Regulation, Neoplastic;
Humans;
Intracellular Signaling Peptides and Proteins;
genetics;
metabolism;
Kidney Neoplasms;
genetics;
metabolism;
pathology;
Male;
MicroRNAs;
genetics;
Middle Aged;
Protein-Serine-Threonine Kinases;
genetics;
metabolism
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2016;36(6):852-858
- CountryChina
- Language:English
-
Abstract:
Renal cell cancer (RCC) remains one of the most lethal types of cancer in adults. MicroRNAs (miRNAs) play key roles in the pathogenesis of RCC. The role of miR-206 in RCC has not been fully understood. The purpose of this study was to examine the role of miR-206 in the regulation of proliferation and metastasis of RCC and the possible mechanism. miR-206 expression was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) 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 miR-206 in RCC. Luciferase assay was performed to verify the precise target of miR-206. The results showed that the expression of miR-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 miR-206 in RCC tissues as well as RCC cell lines. In addition, the miR-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 miR-206 inhibited the expression of GAK. Moreover, miR-206 regulates RCC cell growth partly through targeting GAK. Our study indicated that miR-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.
