Journal
CANCERS
Volume 11, Issue 7, Pages -Publisher
MDPI
DOI: 10.3390/cancers11070955
Keywords
oxidative stress; antioxidants; ROS; NADPH
Categories
Funding
- PRCRP Horizon award by the Department of Defense [W81XWH-17-1-0497]
- NCI [2R01CA131045, 1R01CA174836]
- Pancreatic Cancer Action Network/AACRPathway to Leadership award [13-70-25-LYSS]
- Damon Runyon Cancer Research Foundation [DFS-09-14]
- V Foundation for Cancer Research [V2016-009]
- Sidney Kimmel Foundation for Cancer Research [SKF-16-005]
- 2017 AACR NextGen Grant for Transformative Cancer Research [17-20-01-LYSS]
- ACS Research Scholar Grant [RSG-18-186-01]
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Reactive oxygen species (ROS) are chemically active free radicals produced by partial reduction of oxygen that can activate discrete signaling pathways or disrupt redox homeostasis depending on their concentration. ROS interacts with biomolecules, including DNA, and can cause mutations that can transform normal cells into cancer cells. Furthermore, certain cancer-causing mutations trigger alterations in cellular metabolism that can increase ROS production, resulting in genomic instability, additional DNA mutations, and tumor evolution. To prevent excess ROS-mediated toxicity, cancer-causing mutations concurrently activate pathways that manage this oxidative burden. Hence, an understanding of the metabolic pathways that regulate ROS levels is imperative for devising therapies that target tumor cells. In this review, we summarize the dual role of metabolism as a generator and inhibitor of ROS in cancer and discuss current strategies to target the ROS axis.
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