Mitochondrial ROS generation for regulation of autophagic pathways in cancer

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• 作者：Zi-yue Li^a ;   ; ¹ ; Yu Yang^b ;   ; ¹ ; Miao Ming^a ; Bo Liu^a ;   ; ^{liubo2400@163.com}
• 关键词：Mitochondria ; Reactive oxygen species (ROS) ; Autophagy ; Cancer ; Drug
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2011
• 出版时间：14 October 2011
• 年：2011
• 卷：414
• 期：1
• 页码：5-8
• 全文大小：636 K

文摘

Mitochondria, the main source of reactive oxygen species (ROS), are required for cell survival; yet also orchestrate programmed cell death (PCD), referring to apoptosis and autophagy. Autophagy is an evolutionarily conserved lysosomal degradation process implicated in a wide range of pathological processes, most notably cancer. Accumulating evidence has recently revealed that mitochondria may generate massive ROS that play the essential role for autophagy regulation, and thus sealing the fate of cancer cell. In this review, we summarize mitochondrial function and ROS generation, and also highlight ROS-modulated core autophagic pathways involved in ATG4¨CATG8/LC3, Beclin-1, p53, PTEN, PI3K¨CAkt¨CmTOR and MAPK signaling in cancer. Therefore, a better understanding of the intricate relationships between mitochondrial ROS and autophagy may ultimately allow cancer biologists to harness mitochondrial ROS-mediated autophagic pathways for cancer drug discovery.