Topic Highlight
Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Aug 7, 2016; 22(29): 6619-6628
Published online Aug 7, 2016. doi: 10.3748/wjg.v22.i29.6619
Inflammatory microenvironment contributes to epithelial-mesenchymal transition in gastric cancer
Hui-Ying Ma, Xin-Zhou Liu, Chun-Min Liang
Hui-Ying Ma, Xin-Zhou Liu, Chun-Min Liang, Lab of Tumor Immunology, Department of Anatomy and Histology and Embryology, Shanghai Medical College of Fudan University, Shanghai 200032, China
Author contributions: Ma HY and Liu XZ collected data and drafted the manuscript; Liang CM supervised and revised the manuscript.
Supported by National Science Foundation of China, No. 31471147.
Conflict-of-interest statement: The authors certify that there is no actual or potential conflict of interest and publication copyright in relation to this article.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Chun-Min Liang, MD, PhD, Lab of Tumor Immunology, Department of Anatomy and Histology and Embryology, Shanghai Medical College of Fudan University, 138 Yixueyuan Road, Shanghai 200032, China. cmliang@fudan.edu.cn
Telephone: +86-21-54237027 Fax: +86-21-54237027
Received: March 28, 2016
Peer-review started: March 28, 2016
First decision: May 30, 2016
Revised: June 12, 2016
Accepted: July 6, 2016
Article in press: July 6, 2016
Published online: August 7, 2016
Processing time: 123 Days and 19.9 Hours
Abstract

Gastric cancer (GC) is the fifth most common malignancy in the world. The major cause of GC is chronic infection with Helicobacter pylori (H. pylori). Infection with H. pylori leads to an active inflammatory microenvironment that is maintained by immune cells such as T cells, macrophages, natural killer cells, among other cells. Immune cell dysfunction allows the initiation and accumulation of mutations in GC cells, inducing aberrant proliferation and protection from apoptosis. Meanwhile, immune cells can secrete certain signals, including cytokines, and chemokines, to alter intracellular signaling pathways in GC cells. Thus, GC cells obtain the ability to metastasize to lymph nodes by undergoing the epithelial-mesenchymal transition (EMT), whereby epithelial cells lose their epithelial attributes and acquire a mesenchymal cell phenotype. Metastasis is a leading cause of death for GC patients, and the involved mechanisms are still under investigation. In this review, we summarize the current research on how the inflammatory environment affects GC initiation and metastasis via EMT.

Keywords: Gastric cancer; Inflammation; Epithelial-mesenchymal transition; Microenvironment; Immune cells

Core tip: The major cause of gastric cancer (GC) is Helicobacter pylori infection, resulting in an inflammatory microenvironment in GC. Meanwhile, the leading cause of death for GC patients is metastasis. The major pathway for metastasis is the epithelial-mesenchymal transition (EMT). Therefore, a thorough understanding of how the inflammatory microenvironment contributes to the promotion of the EMT is indispensable for developing new treatments. In this review, we summarize the mechanisms of inflammatory mediators, divided among immune cells and molecules, on the prognosis of GC patients and EMT, which suggests that a combination of immunotherapy and anti-EMT treatments may be encouraging for the treatment of GC.