Pathogenic mechanisms of the oncoprotein CagA in H. pylori-induced gastric cancer

被引：39
作者：
Chen, Shuai-Yin [1 ]
Zhang, Rong-Guang [1 ]
Duan, Guang-Cai [1 ]
机构：
[1] Zhengzhou Univ, Coll Publ Hlth, Dept Epidemiol & Biostat, 100 Kexue Ave, Zhengzhou 450001, Henan, Peoples R China
来源：
ONCOLOGY REPORTS | 2016年 / 36卷 / 06期
关键词：
Helicobacter pylori; CagA; gastric cancer; phosphorylation; epigenetic modifications; VIRULENCE FACTOR CAGA; IV SECRETION SYSTEM; BETA-CATENIN SIGNAL; HELICOBACTER-PYLORI; EPITHELIAL-CELLS; TYROSINE PHOSPHORYLATION; PROMOTER HYPERMETHYLATION; DNA METHYLATION; E-CADHERIN; C-MET;
D O I：
10.3892/or.2016.5145
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Infection with Helicobacter pylori is the strongest risk factor for the development of chronic gastritis, gastric ulcer and gastric carcinoma. The majority of the H. pylori infected population remains asymptomatic, and only 1% of individuals may progress to gastric cancer. The clinical outcomes caused by H. pylori infection are considered to be associated with bacterial virulence, genetic polymorphism of hosts as well as environmental factors. Most H. pylori strains possess a cytotoxin-associated gene (cag) pathogenicity island (cagPAI), encoding a 120-140 kDa CagA protein, which is the most important bacterial oncoprotein. CagA is translocated into host cells via T4SS system and affects the expression of signaling proteins in a phosphorylation-dependent and independent manner. Thus, this review summarizes the results of relevant studies, discusses the pathogenesis of CagA-mediated gastric cancer.
引用
收藏
页码：3087 / 3094
页数：8
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