Metabolic Regulation of Redox Balance in Cancer

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 tran...

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Main Authors: Vinee Purohit, Diane M. Simeone, Costas A. Lyssiotis
Format: Article
Language:English
Published: MDPI AG 2019-07-01
Series:Cancers
Subjects:
Online Access:https://www.mdpi.com/2072-6694/11/7/955
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author Vinee Purohit
Diane M. Simeone
Costas A. Lyssiotis
author_facet Vinee Purohit
Diane M. Simeone
Costas A. Lyssiotis
author_sort Vinee Purohit
collection DOAJ
description 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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spelling doaj.art-62748429084a4c2e9bc793aa9376198b2023-09-02T08:29:40ZengMDPI AGCancers2072-66942019-07-0111795510.3390/cancers11070955cancers11070955Metabolic Regulation of Redox Balance in CancerVinee Purohit0Diane M. Simeone1Costas A. Lyssiotis2Perlmutter Cancer Center, New York University, New York, NY 10016, USAPerlmutter Cancer Center, New York University, New York, NY 10016, USADepartments of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USAReactive 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.https://www.mdpi.com/2072-6694/11/7/955oxidative stressantioxidantsROSNADPH
spellingShingle Vinee Purohit
Diane M. Simeone
Costas A. Lyssiotis
Metabolic Regulation of Redox Balance in Cancer
Cancers
oxidative stress
antioxidants
ROS
NADPH
title Metabolic Regulation of Redox Balance in Cancer
title_full Metabolic Regulation of Redox Balance in Cancer
title_fullStr Metabolic Regulation of Redox Balance in Cancer
title_full_unstemmed Metabolic Regulation of Redox Balance in Cancer
title_short Metabolic Regulation of Redox Balance in Cancer
title_sort metabolic regulation of redox balance in cancer
topic oxidative stress
antioxidants
ROS
NADPH
url https://www.mdpi.com/2072-6694/11/7/955
work_keys_str_mv AT vineepurohit metabolicregulationofredoxbalanceincancer
AT dianemsimeone metabolicregulationofredoxbalanceincancer
AT costasalyssiotis metabolicregulationofredoxbalanceincancer