Reactive oxygen species: A double-edged sword in oncogenesis

被引:264
作者
Pan, Jin-Shui [1 ,2 ,3 ]
Hong, Mei-Zhu [4 ]
Ren, Jian-Lin [1 ,2 ,3 ]
机构
[1] Xiamen Univ, Div Gastroenterol, Zhongshan Hosp, Xiamen 361004, Fujian Province, Peoples R China
[2] Xiamen Univ, Gastroenterol Inst, Xiamen 361004, Fujian Province, Peoples R China
[3] Gastroenterol Ctr Xiamen, Xiamen 361004, Fujian Province, Peoples R China
[4] 174th Hosp PLA, Div Infect Dis, Xiamen 361003, Fujian Province, Peoples R China
基金
中国国家自然科学基金;
关键词
p38 mitogen-activated protein kinases; Reactive oxygen species; Signal transduction; Tumorigenesis; KINASE-C-DELTA; ACTIVATED PROTEIN-KINASE; PROSTATE-CANCER CELLS; NECROSIS-FACTOR-ALPHA; OXIDATIVE STRESS; SIGNALING PATHWAY; INDUCED APOPTOSIS; PC12; CELLS; P38; MAPK; HEPATOCELLULAR-CARCINOMA;
D O I
10.3748/wjg.15.1702
中图分类号
R57 [消化系及腹部疾病];
学科分类号
100201 [内科学];
摘要
Reactive oxygen species (ROS) are molecules or ions formed by the incomplete one-electron reduction of oxygen. Of interest, it seems that ROS manifest dual roles, cancer promoting or cancer suppressing, in tumorigenesis. ROS participate simultaneously in two signaling pathways that have inverse functions in tumorigenesis, Ras-Raf-MEK1/2-ERK1/2 signaling and the p38 mitogen-activated protein kinases (MAPK) pathway. It is well known that Ras-Raf-MEK1/2-ERK1/2 signaling is related to oncogenesis, while the p38 MAPK pathway contributes to cancer suppression, which involves oncogene-induced senescence, inflammation-induced cellular senescence, replicative senescence, contact inhibition and DNA-damage responses. Thus, ROS may not be an absolute carcinogenic factor or cancer suppressor. The purpose of the present review is to discuss the dual roles of ROS in the pathogenesis of cancer, and the signaling pathway mediating their role in tumorigenesis. (C) 2009 The WIG Press and Baishideng. All rights reserved.
引用
收藏
页码:1702 / 1707
页数:6
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