| Literature DB >> 32649885 |
John D Hayes1, Albena T Dinkova-Kostova2, Kenneth D Tew3.
Abstract
Contingent upon concentration, reactive oxygen species (ROS) influence cancer evolution in apparently contradictory ways, either initiating/stimulating tumorigenesis and supporting transformation/proliferation of cancer cells or causing cell death. To accommodate high ROS levels, tumor cells modify sulfur-based metabolism, NADPH generation, and the activity of antioxidant transcription factors. During initiation, genetic changes enable cell survival under high ROS levels by activating antioxidant transcription factors or increasing NADPH via the pentose phosphate pathway (PPP). During progression and metastasis, tumor cells adapt to oxidative stress by increasing NADPH in various ways, including activation of AMPK, the PPP, and reductive glutamine and folate metabolism.Entities:
Keywords: AP-1; BACH1; FOXO; HIF-1alpha; HSF1; NADPH generation; NF-κB; NRF2; PGC-1alpha; TP53; adaptation; antioxidant; dormant cancer cell; folate metabolism; glutathione; initiation; metastasis; oxidative stress; pentose phosphate pathway; progression; reactive oxygen species; recurrent disease; redox signaling; reductive glutamine metabolism; thioredoxin; tumorigenesis
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Year: 2020 PMID： 32649885 PMCID： PMC7439808 DOI： 10.1016/j.ccell.2020.06.001
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743