Involvement of Mitochondrial Reactive Oxygen Species in Gastric CarcinogenesisMasato Tamura1, Michihiro Mutoh2, Gen Fujii2, and Hirofumi Matsui1*
- *Corresponding Author:
- Hirofumi Matsui
Faculty of Medicine, University of Tsukuba 1-1-1 Ten-nohdai
Tsukuba, Ibaraki 305-8573, Japan
E-mail: [email protected]
Received date: July 11, 2013; Accepted date: November 06, 2013; Published date: November 14, 2013
Citation: Tamura M, Mutoh M, Fujii G, Matsui H (2013) Involvement of Mitochondrial Reactive Oxygen Species in Gastric Carcinogenesis. J Gastroint Dig Syst 3:150. doi:10.4172/2161-069X.1000150
Copyright: © 2013 Tamura M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Gastric cancer is one of the most common malignancies in many countries. Environmental gastric cancer risk is known to be associated with Helicobacter pylori infection, a high intake of salty foods, and alcohol consumption. Here, we provide evidence of linkage of mitochondrial reactive oxygen species (ROS) to several environmental gastric cancer risks. Moreover, ROS correlate with gastric cancer invasion and metastasis, the most important factor to decide a patient’s prognosis. We also show correlation between mitochondrial ROS and gastric cancer invasion by using a normal gastric mucosal cell line (RGM-1), a cancerous mutant RGM-1 subclonal (RGK-1) and a MnSOD-expressing RGK-1 cell-line, used for a scavenging mitochondrial ROS. This mini-review summarizes role of ROS in gastric carcinogenesis and aims to provide a clue in developing useful treatments against gastric cancer.