上海交通大学学报（医学版）

上海交通大学学报（医学版） >

2023 , Vol. 43 >Issue 4: 495 - 499

DOI: https://doi.org/10.3969/j.issn.1674-8115.2023.04.013

综述

幽门螺杆菌参与胃癌侵袭转移的研究进展

  • 肖蓉 ,
  • 陶双芬 ,
  • 陈思宇 ,
  • 郑磊贞 ,
  • 朱美玲
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  • 上海交通大学医学院附属新华医院肿瘤科，上海 200092
肖 蓉（1998—），女，硕士生；电子信箱：xrolive98@126.com。
朱美玲，电子信箱：zhumeiling@xinhuamed.com.cn。

收稿日期: 2022-09-01

  录用日期: 2023-03-15

  网络出版日期: 2023-04-28

基金资助

上海市浦江人才计划(2019PJD034)

收起

Advances in Helicobacter pylori infection involved in gastric cancer metastasis

  • Rong XIAO ,
  • Shuangfen TAO ,
  • Siyu CHEN ,
  • Leizhen ZHENG ,
  • Meiling ZHU
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  • Department of Oncology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China
ZHU Meiling, E-mail: zhumeiling@xinhuamed.com.cn.

Received date: 2022-09-01

  Accepted date: 2023-03-15

  Online published: 2023-04-28

Supported by

Shanghai Pujiang Program(2019PJD034)

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摘要

胃癌（gastric cancer，GC）是一种常见的消化道癌症，在东亚和东南亚人群中高发。全球大约有50%以上的人口感染幽门螺杆菌（Helicobacter pylori，HP），HP感染已被证实是GC的致病因素之一，与GC的发生有着密切的关联，与GC侵袭转移的关系虽尚无定论但也有了一定的研究进展。一方面，HP定植胃黏膜后，通过其关键毒力因子空泡细胞毒素A （vacuolating cytotoxin A，VacA）和细胞毒素相关抗原A（cytotoxin-associated antigen A，CagA）的作用使其得以长期存活于胃内，并参与GC细胞的增殖、上皮?间质转化来促进侵袭转移；另一方面，肿瘤微环境作为宿主免疫系统与肿瘤相互作用的场所，HP通过干扰肿瘤微环境内肿瘤细胞与免疫细胞的相互作用、促进肿瘤微环境酸性缺氧环境的形成以及改变微环境内细胞分化等方式，促使GC免疫逃逸从而促进GC的侵袭转移。HP感染如今已成为一个全球性的公共卫生问题，对于GC发生发展的作用更是不容忽视。该文主要围绕上述2个方面，即关键毒力因子和肿瘤微环境来阐述HP感染与GC侵袭转移的相关性，期望能为GC的临床和基础研究提供新思路。

关键词： 胃肿瘤; 幽门螺杆菌; CagA蛋白; VacA蛋白; 肿瘤转移; 免疫逃逸

本文引用格式

肖蓉 , 陶双芬 , 陈思宇 , 郑磊贞 , 朱美玲 . 幽门螺杆菌参与胃癌侵袭转移的研究进展[J]. 上海交通大学学报（医学版）, 2023 , 43(4) : 495 -499 . DOI: 10.3969/j.issn.1674-8115.2023.04.013

Abstract

Gastric cancer is a common cancer of the gastrointestinal tract, highly occurring in East and Southeast Asian. Roughly more than 50% of the population is exposed to Helicobacter pylori (H. pylori) infection worldwide. H. pylori infection is one of the risk factors for gastric cancer and is strongly associated with the development of gastric cancer. The association between H. pylori infection and metastasis of gastric cancer is still inconclusive but has made some progress. For one thing, H. pylori is colonized in the gastric mucosa. The effect of its key virulence factors, VacA and CagA proteins, keeps H. pylori alive in the stomach for a long time and makes it possible for H. pylori to promote the proliferation, epithelial-mesenchymal transition and metastasis of gastric cancer cells. For another, the tumor microenvironment is the site of interaction between host immune system and tumor. By interfering with the effect of tumor cells and immune cells, enhancing the formation of an acidic and hypoxic environment and altering the differentiation of cells in the tumor microenvironment, H. pylori infection can strengthen immune escape and then facilitate the metastasis of gastric cancer. H. pylori infection has become a global public health problem, and its influence on the evolution of gastric cancer cannot be disregarded. The review addresses the correlation between H. pylori infection and gastric cancer metastasis through both key virulence factors and tumor microenvironment. It will provide reference for clinical and basic research in gastric cancer.

Key words： stomach neoplasm; Helicobacter pylori; CagA protein; VacA protein; neoplasm metastasis; immune escape

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