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Oxidative Medicine and Cellular Longevity
Volume 2018, Article ID 5801209, 8 pages
Review Article

Reactive Oxygen Species-Mediated Tumor Microenvironment Transformation: The Mechanism of Radioresistant Gastric Cancer

1Department of Radiation and Medical Oncology, Zhongnan Hospital, Wuhan University, Wuhan, Hubei 430071, China
2Department of Clinical Oncology, First Affiliated Hospital, Medical School of Xi’an Jiaotong University, Xi’an, Shanxi 710061, China
3School of Medicine, University of Texas Medical Branch, Galveston, TX 77555, USA
4Department of Hematology, Zhongnan Hospital, Wuhan University, Wuhan, Hubei 430071, China
5Department of Clinical Pharmacy, Wuhan Union Hospital, Affiliated to Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, China

Correspondence should be addressed to Yongchang Wei; nc.ude.uhw@gnahcgnoyiew

Received 7 October 2017; Revised 30 January 2018; Accepted 26 February 2018; Published 27 March 2018

Academic Editor: Karin Thevissen

Copyright © 2018 Huifeng Gu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Radioresistance is one of the primary causes responsible for therapeutic failure and recurrence of cancer. It is well documented that reactive oxygen species (ROS) contribute to the initiation and development of gastric cancer (GC), and the levels of ROS are significantly increased in patients with GC accompanied with abnormal expressions of multiple inflammatory factors. It is also well documented that ROS can activate cancer cells and inflammatory cells, stimulating the release of a variety of inflammatory cytokines, which subsequently mediates the tumor microenvironment (TME) and promotes cancer stem cell (CSC) maintenance as well as renewal and epithelial-mesenchymal transition (EMT), ultimately resulting in radioresistance and recurrence of GC.