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Cancer Metab. 2014 Nov 28;2:17. doi: 10.1186/2049-3002-2-17. eCollection 2014.

Mitochondrial reactive oxygen species and cancer.

Author information

1
The Koch Institute for Integrative Cancer Research at Massachusetts Institute of Technology, Cambridge, MA 02139 USA.
2
Division of Pulmonary and Critical Care Medicine, Department of Medicine, The Feinberg School of Medicine, Northwestern University, Chicago, IL 60611 USA.

Abstract

Mitochondria produce reactive oxygen species (mROS) as a natural by-product of electron transport chain activity. While initial studies focused on the damaging effects of reactive oxygen species, a recent paradigm shift has shown that mROS can act as signaling molecules to activate pro-growth responses. Cancer cells have long been observed to have increased production of ROS relative to normal cells, although the implications of this increase were not always clear. This is especially interesting considering cancer cells often also induce expression of antioxidant proteins. Here, we discuss how cancer-associated mutations and microenvironments can increase production of mROS, which can lead to activation of tumorigenic signaling and metabolic reprogramming. This tumorigenic signaling also increases expression of antioxidant proteins to balance the high production of ROS to maintain redox homeostasis. We also discuss how cancer-specific modifications to ROS and antioxidants may be targeted for therapy.

KEYWORDS:

Antioxidants; Cancer; Metabolism; Mitochondria reactive oxygen species; Oxidative stress; ROS

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