胃痞消体外抑制胃癌前病变细胞和胃癌SGC7901细胞上皮-间质转化的机制

Inhibitory effect of Weipixiao on epithelial-mesenchymal transition of GPL model cells and gastric cancer cells SGC7901 in vitro

目的:探讨胃痞消(WPX)抑制胃癌前病变细胞和胃癌细胞SGC7901上皮-间质转化(EMT)机制。方法:取人胃黏膜上皮细胞(GES-1)及胃癌细胞SGC7901,MNNG造模及WPX干预后,检测EMT相关分子标志物及细胞迁移力。结果:与空白组比较,模型组SGC7901迁移速度明显加快(P<0.01);与模型组比较,WPX高、低剂量组细胞迁移速度减慢(P<0.01)。模型组E-cad基因表达下调(P<0.05),SGC7901细胞中WPX高、低剂量组VIMENTIN表达较模型组显著降低(P<0.01)。结论:MNNG可诱导SGC7901出现EMT现象,WPX可在一定程度上下调EMT相关基因表达而抑制细胞迁移;同时胃黏膜钙黏分子可与其他分子产生协同机制影响病变细胞持续增殖、炎性反应而延缓进展。

Objective:To investigate the inhibitory effects of Weipixiao(WPX)on the epithelial-mesenchymal transition(EMT)of gastric cancer cells SGC7901 and precancerous lesions.Methods:Human gastric mucosal epithelial cells(GES-1)and gastric cancer cells SGC7901 were used to establish MNNG model.After WPX intervention,EMT-related molecular markers and cell migration were detected.Results:The migration rate of the model group SGC7901 was significantly accelerated compared with the blank group(P<0.01).Compared with the model group,the cell migration rate slowed down in WPX concentration(P<0.01).The expression of E-cad gene was down-regulated(P<0.05),and VIMENTIN of SGC7901 in the high and low dose WPX group was significantly lower than that in the model group(P<0.01).Conclusion:MNNG can induce EMT phenomenon in SGC7901,WPX can down-regulate the expression of EMT-related genes to some extent and inhibit cell migration.The synergistic mechanism of other molecules affects the continuous proliferation and inflammation of diseased cells and delays the progress.