Effects of acetyl-CoA carboxylase 1 on proliferation, migration and invasion of glioma cell line U87
10.16098/j.issn.0529-1356.2022.03.007
- Author:
Yang WANG
1
;
Chao-Hong LI
1
;
Yu-Zhen LIU
1
;
Bao-Sheng ZHAO
2
;
Chao-Hong LI
2
;
Yu-Zhen LIU
2
Author Information
1. Life Science Research Center, The First Affiliated Hospital of Xinxiang Medical University
2. Department of Thoracic Surgery, The First Affiliated Hospital of Xinxiang Medical University
- Publication Type:Journal Article
- Keywords:
Acetyl-CoA carboxylase 1;
Human;
Invasion;
Migration;
Proliferation;
U87 cell;
Western blotting
- From:
Acta Anatomica Sinica
2022;53(3):317-322
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the effect of acetyl-CoA carboxylase 1(ACC1) on cell proliferation, migration and invasion of human glioma cell line U87. Methods Western blotting was performed to examine endogenous ACC1 expression in human glioma cell lines U87, U251 and U373. ACC1 overexpression plasmid and the plasmid vector were transiently transfected into U87 cells. The level of ACC1 in control and ACC1 overexpression cells was examined by Western blotting. The effect of ACC1 on U87 cells migration and invasion was detected by Transwell assay. The effect of ACC1 on U87 cells scratch healing ability was detected by scratch test. The effect of ACC1 on U87 cells proliferation was investigated by MTT assay. Western blotting was conducted to detect the level changes of proteins. Results Among three human glioma cell lines U87, U251 and U373, endogenous ACC1 level in U87 cells was lower than that in other two cell lines. ACC1 overexpression inhibited U87 cell proliferation, as well as cell migration, invasion and scratch healing ability (P < 0.05). Vimentin, fibronectin, urokinase type plasminogen activator (uPA), Bcl-2, cyclin B, cyclin D and p-STAT3 were down-regulated (P< 0.05), P21 was up-regulated (P < 0.05) after ACC1 overexpression. Conclusion These results suggest that ACC1 suppresses the proliferation, migration and invasion of human glioma cells, probably by inhibiting STAT3 activity.
