Mitochondrial reactive oxygen species and cancer
Author(s)
Chandel, Navdeep S; Sullivan, Lucas Bryan
Download2049-3002-2-17.pdf (813.8Kb)
PUBLISHER_CC
Publisher with Creative Commons License
Creative Commons Attribution
Terms of use
Metadata
Show full item recordAbstract
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.
Date issued
2014-11Department
Koch Institute for Integrative Cancer Research at MITJournal
Cancer & Metabolism
Publisher
BioMed Central Ltd
Citation
Sullivan, Lucas B, and Navdeep S Chandel. “Mitochondrial Reactive Oxygen Species and Cancer.” Cancer & Metabolism 2.1 (2014): 17.
Version: Final published version
ISSN
2049-3002