The DOI matches its Crossref record; 114 of the 114 references it cites were found in a registry or an index.
Mitochondrial reactive oxygen species and cancer
Open accessAbstract
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.
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Cites
1 retracted
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RetractedHow mitochondria produce reactive oxygen species
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Cited by
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Metadata
- Authors
- Sullivan, L. B., & Chandel, N. S.
- Venue
- Cancer & Metabolism
- Published
- 2014-11-28
- Volume
- 2
- Issue
- 1
- Pages
- 17-17
- ISSN
- 2049-3002 (ISSN-L)
- OpenAlex
- W2133032371
- Cited by
- 786
- References
- 114
- FWCI
- 18.98
- Type
- journal article
- Language
- en
- Open access
- gold
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
