Metabolic Regulation of Redox Balance in Cancer

Vinee Purohit; Diane M Simeone; Costas A Lyssiotis

doi:10.3390/cancers11070955

Metabolic Regulation of Redox Balance in Cancer

Cancers (Basel). 2019 Jul 8;11(7):955. doi: 10.3390/cancers11070955.

Authors

Vinee Purohit¹, Diane M Simeone^{1

2

3}, Costas A Lyssiotis^{4

5

6}

Affiliations

¹ Perlmutter Cancer Center, New York University, New York, NY 10016, USA.
² Department of Surgery, New York University, New York, NY 10016, USA.
³ Department of Pathology, New York University, New York, NY 10016, USA.
⁴ Departments of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA. clyssiot@med.umich.edu.
⁵ Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA. clyssiot@med.umich.edu.
⁶ Rogel Cancer Center, University of Michigan, Ann Arbor, MI 48109, USA. clyssiot@med.umich.edu.

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.

Keywords: NADPH; ROS; antioxidants; oxidative stress.

Publication types

Review

Abstract

Publication types

Grants and funding