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活性氧:肿瘤发生中的双刃剑。

Reactive oxygen species: a double-edged sword in oncogenesis.

作者信息

Pan Jin-Shui, Hong Mei-Zhu, Ren Jian-Lin

机构信息

Division of Gastroenterology, Zhongshan Hospital Xiamen University, Fujian Province, China.

出版信息

World J Gastroenterol. 2009 Apr 14;15(14):1702-7. doi: 10.3748/wjg.15.1702.

Abstract

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.

摘要

活性氧(ROS)是由氧的不完全单电子还原形成的分子或离子。有趣的是,ROS在肿瘤发生过程中似乎表现出促进癌症或抑制癌症的双重作用。ROS同时参与两条在肿瘤发生中具有相反功能的信号通路,即Ras-Raf-MEK1/2-ERK1/2信号通路和p38丝裂原活化蛋白激酶(MAPK)通路。众所周知,Ras-Raf-MEK1/2-ERK1/2信号通路与肿瘤发生有关,而p38 MAPK通路则有助于癌症抑制,这涉及癌基因诱导的衰老、炎症诱导的细胞衰老、复制性衰老、接触抑制和DNA损伤反应。因此,ROS可能不是绝对的致癌因素或癌症抑制因子。本综述的目的是讨论ROS在癌症发病机制中的双重作用,以及介导其在肿瘤发生中作用的信号通路。

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