Injury of human gastric epithelial GES-1 cells by MNNG and its effects on Wnt/β-catenin signaling pathway.
- Author:
Zhan-Peng YAN
1
;
Ting-Ting XU
1
;
Zhen-Tao AN
1
;
Ying HU
1
;
Wan-Zhen CHEN
1
;
Fang-Shi ZHU
2
Author Information
1. Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing 210028, China.
2. Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing 210028, China. zhufangshi@126.com.
- Publication Type:Journal Article
- From:
Acta Physiologica Sinica
2018;70(3):262-268
- CountryChina
- Language:Chinese
-
Abstract:
The aim of this study was to investigate the mechanisms of mono-functional alkylating agent MNNG to damage human gastric epithelial GES-1 cells and roles of Wnt/β-catenin signaling pathway in the process. The GES-1 cells were treated with MNNG (2 × 10 mol/L) for 24 h. The morphological changes of the GES-1 cells were observed under inverted microscope 2 d after treatment. The cell viability was measured by MTT assay. The apoptosis and cell cycle distribution of the GES-1 cells were analyzed by flow cytometry. The mRNA expressions of β-catenin, GSK-3β, c-Met and MMP7 in the GES-1 cells were detected by qPCR. The protein expressions of β-catenin, GSK-3β, p-GSK-3β and c-Met were determined by Western blot. The results showed that MNNG induced the injury of GES-1 cells and changed the normal cell morphology to irregular long spindle shape. MNNG induced the apoptosis of GES-1 cells and blocked the cell cycle progression obviously. MNNG up-regulated the mRNA expressions of β-catenin, GSK-3β, c-Met and MMP7, and increased the protein expressions of β-catenin, GSK-3β and p-GSK-3β. These results suggest that the damage of GES-1 cells induced by MNNG may be related to the activation of Wnt/β-catenin signaling pathway, which will provide the basis for the study of cell model of gastric mucosal cell injury.
