lncRNA MAFG-AS1 promotes migration, invasion and aerobic glycolysis of gastric cancer AGS cells by regulating miR-11181-3p/GLG1 axis
10.3872/j.issn.1007-385x.2020.09.005
- VernacularTitle:lncRNA MAFG-AS1通过调控miR-11181-3p/GLG1轴促进胃癌AGS细 胞迁移、侵袭和有氧糖酵解
- Author:
QIAN Cuijuan
1
;
XU Zhurong
1
;
CHEN Luyan
1
;
SUN Yao
1
;
YAO Jun
1
Author Information
1. (a. Medical College, b. Institute of Tumor, Taizhou University, Taizhou 318000, Zhejiang, China
- Publication Type:Journal Article
- Keywords:
gastric cancer;
AGS cells;
lncRNA;
MAFG-AS1;
aerobic glycolysis;
invasion
- From:
Chinese Journal of Cancer Biotherapy
2020;27(9):992-998
- CountryChina
- Language:Chinese
-
Abstract:
[Abstract] Objective: To investigate the effect of lncRNA MAFG-AS1/ miR-11181-3p/GLG1 axis on cell migration, invasion and aerobic glycolysis of gastric cancer (GC) cells and its possible mechanism. Methods: AGS, a GC cell line with relatively high expression of MAFG-AS1, was selected as the study object. qPCR was used to detect RNA expression levels of MAFG-AS1, miR-11181-3p and GLG1. Transwell and glycolysis analysis were used to investigate cell migration, invasion and aerobic glycolysis. Bioinformatics analysis and Dual luciferase reporter gene assay were used to analyze the interaction among MAFG-AS1, miR-11181-3p and GLG1. Results: Knockdown of MAFG-AS1 significantly up-regulated miR-11181-3p and down-regulated GLG1 expression (both P<0.01), and significantly inhibited migration, invasion and aerobic glycolysis of GC cells (all P<0.01). Luciferase reporter gene assay confirmed that MAFG-AS1 competitively sponged miR-11181-3p (P<0.01). Inhibition of miR-11181-3p or overexpression of GLG1 partially reversed the inhibitory effect of MAFG-AS1 knockdown on GC cell migration, invasion, and aerobic glycolysis (all P<0.05 or P<0.01). Conclusion: MAFG-AS1 promotes cell migration, invasion and aerobic glycolysis of GC cells via miR-11181-3p/GLG1 axis, and may be a potential molecular target for GC diagnosis and therapy.
- Full text:20200905.pdf