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.
Highlights
Oxygen (O2 ) is indispensable for the survival of eukaryotic organisms that use it to generate the energy currency adenosine triphosphate (ATP)
Generation, cancer cells increase the activity of antioxidant synthesis pathways, which enables them to survive in a microenvironment that is otherwise unfriendly to most normal adult cells
In the section that follows, we provide an overview of these three three antioxidant classes, present the thatlead leadtoto their function regulation, antioxidant classes, present themetabolic metabolic pathways pathways that their function andand regulation, including but not limited to
Summary
Oxygen (O2 ) is indispensable for the survival of eukaryotic organisms that use it to generate the energy currency adenosine triphosphate (ATP). Recent studies have unfurled the role of ROS as signaling intermediates whose production and regulation are controlled processes with biological significance [1]. Transformation of cells to a malignant state causes a surge in ROS production, due to activation of oncogenes, loss of tumor suppressors, alterations in the expression, and/or assembly of mitochondrial electron transport chain (ETC) enzymes and through interaction with factors and conditions in the tumor microenvironment [4,5,6,7]. Cancer cells require mechanisms to balance this hyperactive ROS machinery. Concomitant to increased ROS generation, cancer cells increase the activity of antioxidant synthesis pathways, which enables them to survive in a microenvironment that is otherwise unfriendly to most normal adult cells.
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