Year: 2019
Type: review
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.
Source: Cancers
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $1,824
Funders: U.S. Department of Defense, American Association for Cancer Research, American Cancer Society, Damon Runyon Cancer Research Foundation, V Foundation for Cancer Research, Pancreatic Cancer Action Network, Sidney Kimmel Foundation for Cancer Research, Sidney Kimmel Foundation, Servier, National Cancer Institute, DOD Peer Reviewed Cancer Research Program
Awards: G1246052488, G1788178761, G2040153736, G2826248725, G3412212806, G4119534169, G4154711967, Oncogenic Function of ATDC in Bladder Cancer, G5876317186, ROLE OF ATDC IN THE REGULATION OF ANTIOXIDANT RESPONSE IN PANCREATIC CANCER, Early Detection Biomarkers in Pancreatic Adenocarcinoma, G8299130710
OpenAlex ID: W2954634684