Mechanism of chlorogenic acid in apoptotic regulation through AKT/GSK-3βpathway in colon cancer cell
10.3760/cma.j.issn.1673-4181.2017.06.005
- VernacularTitle:绿原酸通过AKT/GSK-3β信号通路调控结肠癌细胞凋亡及机制
- Author:
Chenyun LI
1
;
Tong SUN
;
Na ZHUO
;
Jing TIAN
Author Information
1. 300211,天津医科大学第二医院超声科
- Keywords:
Colon cancer;
Chlorogenic acid;
AKT/GSK-3βpathways;
Proliferation;
Apoptosis
- From:
International Journal of Biomedical Engineering
2017;40(6):426-431
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the regulation mechanism of chlorogenic acid (CGA) on proliferation and apoptosis of colon cancer cell. Methods The effect of CGA with different concentrations on the apoptosis of human colon cancer cell line HT-29 was detected by flow cytometry, the cell proliferation was detected by MTT assay, and the cell migration was detected by Transwell method. The nude mice tumor model of HT-29 cells was established by injecting 100μl CGA (100μg/ml) into the tumor area, and 100μl saline was injected into the same area of control group. The tumor volume and quality were measured periodically. The expression level of AKT/GSK-3β signaling pathway was detected by Western Blot. Results CGA can significantly promote the apoptosis of HT-29 cells (P<0.01), significantly inhibit the cell proliferation ( P<0 . 01 ) and cell migration ( P<0 . 05 ) . These effects showed a dose-dependent tendency. The CGA-treated HT-29 tumor-bearing mice developed no metastases in vivo. At the different time points, the tumor volume and weight of the experimental group were significantly smaller than those of the control group (all P<0.05). There were no significant differences in the expression of AKT and GSK-3 between the two groups (all P>0.05). The phosphorylated proteins (p-AKT and p-GSK-3) andβ-catenin in the experimental group were significantly lower than those in the control group (all P<0.01). Conclusion CGA can inhibit the proliferation and metastasis of colon cancer cells, and promote apoptosis. This mechanism might involve AKT/GSK-3βpathways.
