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Sheng Li Xue Bao ; 70(3): 262-268, 2018 Jun 25.
Artigo em Chinês | MEDLINE | ID: mdl-29926067

RESUMO

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/ß-catenin signaling pathway in the process. The GES-1 cells were treated with MNNG (2 × 10-5 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 ß-catenin, GSK-3ß, c-Met and MMP7 in the GES-1 cells were detected by qPCR. The protein expressions of ß-catenin, GSK-3ß, p-GSK-3ß 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 ß-catenin, GSK-3ß, c-Met and MMP7, and increased the protein expressions of ß-catenin, GSK-3ß and p-GSK-3ß. These results suggest that the damage of GES-1 cells induced by MNNG may be related to the activation of Wnt/ß-catenin signaling pathway, which will provide the basis for the study of cell model of gastric mucosal cell injury.


Assuntos
Células Epiteliais/efeitos dos fármacos , Células Epiteliais/metabolismo , Metilnitronitrosoguanidina/efeitos adversos , Via de Sinalização Wnt , Apoptose , Ciclo Celular , Linhagem Celular , Sobrevivência Celular , Mucosa Gástrica/citologia , Quinase 3 da Glicogênio Sintase/metabolismo , Glicogênio Sintase Quinase 3 beta , Humanos , Metaloproteinase 7 da Matriz/metabolismo , Proteínas Proto-Oncogênicas c-met/metabolismo , beta Catenina/metabolismo
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