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Cancers (Basel). 2016 Mar 25;8(4). pii: E40. doi: 10.3390/cancers8040040.

Mitochondrial Redox Signaling and Tumor Progression.

Author information

1
The First Affiliated Hospital, Center for Translational Medicine, Sun Yat-sen University, Guangzhou 510080, China. yuxin_chen2015@163.com.
2
The First Affiliated Hospital, Center for Translational Medicine, Sun Yat-sen University, Guangzhou 510080, China. qingzh123@163.com.
3
Interdepartmental Program in Vascular Biology and Therapeutics, Department of Pathology, Yale University School of Medicine, 10 Amistad St, New Haven, CT 06520, USA. huanjiao.zhou@yale.edu.
4
The First Affiliated Hospital, Center for Translational Medicine, Sun Yat-sen University, Guangzhou 510080, China. wdji2008@126.com.
5
The First Affiliated Hospital, Center for Translational Medicine, Sun Yat-sen University, Guangzhou 510080, China. wang.min@yale.edu.
6
Interdepartmental Program in Vascular Biology and Therapeutics, Department of Pathology, Yale University School of Medicine, 10 Amistad St, New Haven, CT 06520, USA. wang.min@yale.edu.

Abstract

Cancer cell can reprogram their energy production by switching mitochondrial oxidative phosphorylation to glycolysis. However, mitochondria play multiple roles in cancer cells, including redox regulation, reactive oxygen species (ROS) generation, and apoptotic signaling. Moreover, these mitochondrial roles are integrated via multiple interconnected metabolic and redox sensitive pathways. Interestingly, mitochondrial redox proteins biphasically regulate tumor progression depending on cellular ROS levels. Low level of ROS functions as signaling messengers promoting cancer cell proliferation and cancer invasion. However, anti-cancer drug-initiated stress signaling could induce excessive ROS, which is detrimental to cancer cells. Mitochondrial redox proteins could scavenger basal ROS and function as "tumor suppressors" or prevent excessive ROS to act as "tumor promoter". Paradoxically, excessive ROS often also induce DNA mutations and/or promotes tumor metastasis at various stages of cancer progression. Targeting redox-sensitive pathways and transcriptional factors in the appropriate context offers great promise for cancer prevention and therapy. However, the therapeutics should be cancer-type and stage-dependent.

KEYWORDS:

anti-oxidant proteins; apoptosis; cancer progression; mitochondria; redox signaling

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