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目的幽门螺杆菌被认为是诱发胃癌的最强的风险因素。幽门螺旋杆菌的毒性成分是可以增加癌症危险的cag分泌系统,它可以使cagA和肽聚糖易位进入宿主细胞,进而激活信号转导通路。AKT是磷脂酰肌醇3-激酶(PI3K)的目的蛋白,并在胃癌中被激活,但PI3K-AKT和具有潜在致癌性的幽门螺旋杆菌诱导的细胞反应之间的关系尚不清楚。方法我们揭示了介导幽门螺旋杆菌刺激的AKT活化和胃上皮细胞的这些生物学结果之间的分子通路。结果幽门螺旋杆菌以Scr和表皮生长因子受体依赖性方式增加PI3K-AKT的信号,是幽门螺旋杆菌诱导的细胞迁移不可或缺的。结论这些结果表明,PI3K-AKT信号调节幽门螺旋杆菌诱发的病理生理反应,从而降低癌变门槛。
Purpose Helicobacter pylori is considered to be the strongest risk factor for gastric cancer. The toxic component of H. pylori is a cag secretion system that increases the risk of cancer by allowing translocation of cagA and peptidoglycan into host cells, which in turn activates signal transduction pathways. AKT is a target protein of phosphatidylinositol 3-kinase (PI3K) and is activated in gastric cancer, but the relationship between PI3K-AKT and the potentially carcinogenic Helicobacter pylori-induced cellular response is unclear. Methods We revealed the molecular pathways mediating H. pylori-stimulated AKT activation and these biological consequences of gastric epithelial cells. Results H. pylori increased PI3K-AKT signaling in a Scr and epidermal growth factor receptor-dependent manner, which is essential for H. pylori-induced cell migration. Conclusions These results indicate that the PI3K-AKT signal regulates the pathophysiological response induced by H. pylori, thereby reducing the threshold for canceration.