Silencing of Long Non-Coding RNA MALAT1 Promotes Apoptosis of Glioma Cells.
10.3346/jkms.2016.31.5.688
- Author:
Jianping XIANG
1
;
Shifeng GUO
;
Shuling JIANG
;
Yuelong XU
;
Jiwei LI
;
Li LI
;
Jinyu XIANG
Author Information
1. Department of Neurology, Yishui Central Hospital, Shandong, China.
- Publication Type:Original Article
- Keywords:
RNA, Long Noncoding;
MALAT1 Long Non-coding RNA, Human;
Glioma;
Apoptosis
- MeSH:
*Apoptosis;
Biomarkers, Tumor/genetics/metabolism;
Blotting, Western;
Cell Line, Tumor;
Cell Movement;
Cell Proliferation;
Cyclin D1/genetics/metabolism;
Down-Regulation;
Flow Cytometry;
Glioma/metabolism/pathology;
Humans;
Proto-Oncogene Proteins c-myc/genetics/metabolism;
*RNA Interference;
RNA, Long Noncoding/antagonists & inhibitors/genetics/*metabolism;
RNA, Small Interfering/metabolism;
Real-Time Polymerase Chain Reaction
- From:Journal of Korean Medical Science
2016;31(5):688-694
- CountryRepublic of Korea
- Language:English
-
Abstract:
The metastasis-associated lung adenocarcinoma transcription 1 (MALAT1) is a highly conserved long non-coding RNA (lncRNA) gene. However, little is known about the pathological role of lncRNA MALAT1 in glioma. In the present study, we explored the expression level of lncRNA MALAT1 in primary glioma tissues as well as in U87 and U251 glioma cell lines. Using qRT-PCR, we found that the expression of lncRNA MALAT1 was significantly increased in glioma tissues compared with that of paracancerous tissues. Meanwhile, the expression of MALAT1 was highly expressed in U98 and U251 cells. In order to explore the function of MALAT1, the expression of MALAT1 was greatly reduced in U87 and U251 cells transfected with siRNA specifically targeting MALAT1. Consequently, cell viability of U87 and U251 cells were drastically decreased after the knockdown of MALAT1. Concomitantly, the apoptosis rate of the two cell lines was dramatically increased. Furthermore, the expression levels of some tumor markers were reduced after the knockdown of MALAT1, such as CCND1 and MYC. In summary, the current study indicated a promoting role of MALAT1 in the development of glioma cell.
