幽门螺杆菌CagA诱导胃部炎癌转化的研究进展  

Research progress on Helicobacter pylori CagA-induced gastric inflammation-cancer transformation

作　　者：顾晓 邢莹莹[1] GU Xiao;XING Yingying(School of Life Science and Technology,China Pharmaceutical University,Nanjing 211198,China)

机构地区：[1]中国药科大学生命科学与技术学院,南京211100

出　　处：《中国药科大学学报》2025年第1期132-138,共7页Journal of China Pharmaceutical University

基　　金：国家自然科学基金项目(No.81971562);2024年海南省卫生健康科技创新联合项目(WSJK2024MS230)。

摘　　要：幽门螺杆菌(Helicobacter pylori,Hp)目前已被列为能导致胃癌发生的Ⅰ类致病菌,近年来,对于幽门螺杆菌感染如何引起胃癌的发生和发展的研究备受瞩目。细胞毒力相关基因A(CagA)作为Hp的首要毒力因子,目前已经有大量研究报道其可以作为Hp产生胃部感染、定植以及促使宿主细胞发生炎癌转化等的关键外分泌毒素发挥功能,感染CagA阳性菌株的患者相比于CagA阴性菌株感染患者具有更高患肿瘤的概率。本文基于前期研究,从毒力蛋白CagA的递送方式、生物活性、免疫调控以及相关分子机制层面对Hp感染所诱导胃癌的发生以及发展过程进行阐述。Helicobacter pylori(Hp)is currently classified as a class I carcinogen that can cause gastric cancer,research in recent years on how Hp infection causes the occurrence and progression of gastric cancer has attracted much attention.As the primary virulence factor of Hp,cytotoxicity-associated gene A(CagA)has been extensively studied and reported to function as a key excreted toxin for Hp to induce gastric infection,colonization and promote inflammatory-carcinogenic transformation of host cells.Patients infected with CagA-positive strains have a higher risk of developing tumors compared to those infected with CagA-negative strains.Based on previous studies,this article further elaborates on the import process,biological activity,and related molecular mechanisms of virulence protein CagA in the occurrence and development of gastric cancer induced by Hp infection.

关 键 词：胃癌 幽门螺杆菌 CAGA 炎癌转化 分子机制 

分 类 号：R573[医药卫生—消化系统] Q936[医药卫生—内科学]