Long non-coding RNA MEG3 induces renal cell carcinoma cells apoptosis by activating the mitochondrial pathway.
10.1007/s11596-015-1467-5
- Author:
Miao WANG
1
;
Tao HUANG
;
Gang LUO
;
Chao HUANG
;
Xing-Yuan XIAO
;
Liang WANG
;
Guo-Song JIANG
;
Fu-Qing ZENG
Author Information
1. Department of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China, wangmiaotj@163.com.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
Carcinoma, Renal Cell;
genetics;
metabolism;
pathology;
Cell Line, Tumor;
Cell Survival;
Gene Expression Regulation, Neoplastic;
HEK293 Cells;
Humans;
Kidney Neoplasms;
genetics;
metabolism;
pathology;
Mitochondria;
genetics;
RNA, Long Noncoding;
genetics;
metabolism;
Signal Transduction
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2015;35(4):541-545
- CountryChina
- Language:English
-
Abstract:
This study aimed to examine the effect of long non-coding RNA (LncRNA) MEG3 on the biological behaviors of renal cell carcinoma (RCC) cells 786-0 and the possible mechanism. MEG3 expression levels were detected by RT-qPCR in tumor tissues and adjacent non-tumor tissues from 29 RCC patients and in RCC lines 786-0 and SN12 and human embryonic kidney cell line 293T. Plasmids GV144-MEG3 (MEG3 overexpression plasmid) and GV144 (control plasmid) were stably transfected into 786-0 cells by using lipofectamine 2000. Cell viabilities were determined by MTT, cell apoptosis rates by flow cytometry following PE Annexin V and 7AAD staining, apoptosis-related protein expressions by Western blotting, and Bcl-2 mRNA by RT-qPCR in the transfected cells. The results showed that MEG3 was evidently downregulated in RCC tissues (P<0.05) and RCC cell lines (P<0.05). The viabilities of 786-0 cells were decreased significantly after transfection with GV144-MEG3 for over 24 h (P<0.05). Consistently, the apoptosis rate was significantly increased in 786-0 cells transfected with GV144-MEG3 for 48 h (P<0.05). Furthermore, overexpression of MEG3 could reduce the expression of Bcl-2 and procaspase-9 proteins, enhance the expression of cleaved caspase-9 protein, and promote the release of cytochrome c protein to cytoplasm (P<0.05). Additionally, Bcl-2 mRNA level was declined by MEG3 overexpression (P<0.05). It was concluded that MEG3 induces the apoptosis of RCC cells possibly by activating the mitochondrial pathway.
