Glycogen synthase kinase 3beta induces cell cycle arrest in a cyclin D1-dependent manner in human lung adenocarcinoma cell line A549.
- Author:
Jian-Sha LI
1
;
Min ZHU
;
Dan TIAN
;
Man-Xiang WANG
;
Fang WANG
;
Na-Ping LI
;
Ren-Liang WU
Author Information
1. Department of Pathology, Tongji Medical College, Huazhong University of Science and Technology, and Key Laboratory of Pulmonary Disease of Ministry of Health of China, Wuhan, China.
- Publication Type:Journal Article
- MeSH:
Adenocarcinoma;
pathology;
Cell Cycle Checkpoints;
Cell Line, Tumor;
Cell Proliferation;
Cyclin D1;
metabolism;
Down-Regulation;
Glycogen Synthase Kinase 3;
metabolism;
Glycogen Synthase Kinase 3 beta;
Humans;
Lung Neoplasms;
pathology;
Transfection
- From:
Acta Physiologica Sinica
2007;59(2):204-209
- CountryChina
- Language:English
-
Abstract:
The effect of glycogen synthase kinase 3beta (GSK3beta) has been repeatedly implicated in cell proliferation, but studies on the effect of GSK3beta in different cell lines with different stimuli have drawn different conclusions. To investigate the direct effect of GSK3beta on cell growth in human lung adenocarcinoma cell line A549, we changed its activity by transient transfection with two kinds of GSK3beta mutant plasmids, constitutively active form S9A-GSK3beta and dominant negative form KM-GSK3beta. Twenty-four hours later, cell counting, flow cytometry and Western blot detection were made respectively. The results showed that enhancing GSK3beta activity caused a decrease in cell number, as well as a higher percentage of cells at G(1) phase. Further, the expression of cyclin D1 was down-regulated by GSK3beta. Taken together, our observations suggest that GSK3beta may induce G(1) cell cycle arrest in a cyclin D1-dependent fashion and therefore possibly plays a growth-inhibitory role in A549 cells.
