Metabolic Regulation of Redox Balance in Cancer
Abstract
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.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Jul 08, 2019
- Source ID
- 10.3390/cancers11070955
Entities
People
- Costas A Lyssiotis
- Diane M. Simeone
- Vinee Purohit
Organizations
- American Association for Cancer Research
- American Cancer Society
- Damon Runyon Cancer Research Foundation
- National Cancer Institute
- Pancreatic Cancer Action Network
- Sidney Kimmel Foundation
- United States Department of Defense
- V Foundation for Cancer Research