胃癌(GC),一种常见且高死亡率的疾病,在目前的癌症研究中仍占有重要地位,和幽门螺杆菌(H.pylori)感染作为其重要的危险因素一直是一个热点和具有挑战性的研究领域。在幽门螺杆菌的众多致病因素中,毒力蛋白CagA已被广泛研究为唯一的细菌来源的癌蛋白。发现CagA进入胃上皮细胞(GECs)可诱导MAPK信号通路等多种细胞通路的失调,PI3K/Akt信号通路,NF-κB信号通路,Wnt/β-catenin信号通路,JAK-STAT信号通路,Hippo信号通路通过磷酸化和非磷酸化。这些紊乱的通路引起形态学的病理变化,附着力,极性,扩散,运动,和GEC的其他过程,最终促进了GC的发生。随着H.pylori相关研究的不断深入,CagA诱导异常信号通路的研究在一定程度上得到了更新和深化,因此本文以CagA激活的关键信号通路为主要茎,旨在为将来幽门螺杆菌感染和治疗GC提供新的策略。
Gastric cancer (GC), a common and high-mortality disease, still occupies an important position in current cancer research, and Helicobacter pylori (H. pylori) infection as its important risk factor has been a hot and challenging research area. Among the numerous pathogenic factors of H. pylori, the virulence protein CagA has been widely studied as the only bacterial-derived oncoprotein. It was found that CagA entering into gastric epithelial cells (GECs) can induce the dysregulation of multiple cellular pathways such as MAPK signaling pathway, PI3K/Akt signaling pathway, NF-κB signaling pathway, Wnt/β-catenin signaling pathway, JAK-STAT signaling pathway, Hippo signaling pathway through phosphorylation and non-phosphorylation. These disordered pathways cause pathological changes in morphology, adhesion, polarity, proliferation, movement, and other processes of GECs, which eventually promotes the occurrence of GC. With the deepening of H. pylori-related research, the research on CagA-induced abnormal signaling pathway has been updated and deepened to some extent, so the key signaling pathways activated by CagA are used as the main stem to sort out the pathogenesis of CagA in this paper, aiming to provide new strategies for the H. pylori infection and treatment of GC in the future.