Oxidative Stress in Cancer

John Hayes; Albena Dinkova-Kostova; Kenneth D. Tew

doi:10.1016/j.ccell.2020.06.001

Oxidative Stress in Cancer

John Hayes (Lead / Corresponding author), Albena Dinkova-Kostova, Kenneth D. Tew

Cellular Medicine

Research output: Contribution to journal › Review article › peer-review

885 Citations (Scopus)

267 Downloads (Pure)

Abstract

Contingent upon concentration, reactive oxygen species (ROS) influence cancer evolution in apparently contradictory ways, either initiating/stimulating tumorigenesis and supporting transformation/proliferation of cancer cells or causing cell death. To accommodate high ROS levels, tumor cells modify sulfur-based metabolism, NADPH generation and the activity of antioxidant transcription factors. During initiation, genetic changes enable cell survival under high ROS levels by activating antioxidant transcription factors or increasing NADPH via the pentose phosphate pathway (PPP). During progression and metastasis, tumor cells adapt to oxidative stress by increasing NADPH in various ways, including activation of AMPK, the PPP, and reductive glutamine and folate metabolism.

Original language	English
Pages (from-to)	167-197
Number of pages	31
Journal	Cancer Cell
Volume	38
Issue number	2
Early online date	9 Jul 2020
DOIs	https://doi.org/10.1016/j.ccell.2020.06.001
Publication status	Published - 10 Aug 2020

Keywords

oxidative stress
reactive oxygen species
adaptation
glutathione
thioredoxin
NADPH generation
pentose phosphate pathway
reductive glutamine metabolism
folate metabolism
redox signaling
antioxidant
NRF2
BACH1
AP-1
FOXO
PGC-1alpha
HIF-1alpha
HSF1
NF-κB
TP53
tumorigenesis
initiation
progression
metastasis
dormant cancer cell
recurrent disease

ASJC Scopus subject areas

Oncology
Cancer Research
Cell Biology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1016/j.ccell.2020.06.001Licence: Elsevier User Licence

Author Accepted ManuscriptAccepted author manuscript, 421 KBLicence: CC BY-NC-ND

Cite this

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title = "Oxidative Stress in Cancer",

abstract = "Contingent upon concentration, reactive oxygen species (ROS) influence cancer evolution in apparently contradictory ways, either initiating/stimulating tumorigenesis and supporting transformation/proliferation of cancer cells or causing cell death. To accommodate high ROS levels, tumor cells modify sulfur-based metabolism, NADPH generation and the activity of antioxidant transcription factors. During initiation, genetic changes enable cell survival under high ROS levels by activating antioxidant transcription factors or increasing NADPH via the pentose phosphate pathway (PPP). During progression and metastasis, tumor cells adapt to oxidative stress by increasing NADPH in various ways, including activation of AMPK, the PPP, and reductive glutamine and folate metabolism.",

keywords = "oxidative stress, reactive oxygen species, adaptation, glutathione, thioredoxin, NADPH generation, pentose phosphate pathway, reductive glutamine metabolism, folate metabolism, redox signaling, antioxidant, NRF2, BACH1, AP-1, FOXO, PGC-1alpha, HIF-1alpha, HSF1, NF-κB, TP53, tumorigenesis, initiation, progression, metastasis, dormant cancer cell, recurrent disease",

author = "John Hayes and Albena Dinkova-Kostova and Tew, {Kenneth D.}",

note = "We gratefully acknowledge the Medical Research Council (MR/N009851/1, MR/T014644/1), Cancer Research UK (C20953/A18644), National Institutes of Health (5P20GM103542; C06RR015455) and South Carolina Centers of Excellence program for funding",

year = "2020",

month = aug,

day = "10",

doi = "10.1016/j.ccell.2020.06.001",

language = "English",

volume = "38",

pages = "167--197",

journal = "Cancer Cell",

issn = "1535-6108",

publisher = "Elsevier",

number = "2",

}

TY - JOUR

T1 - Oxidative Stress in Cancer

AU - Hayes, John

AU - Dinkova-Kostova, Albena

AU - Tew, Kenneth D.

N1 - We gratefully acknowledge the Medical Research Council (MR/N009851/1, MR/T014644/1), Cancer Research UK (C20953/A18644), National Institutes of Health (5P20GM103542; C06RR015455) and South Carolina Centers of Excellence program for funding

PY - 2020/8/10

Y1 - 2020/8/10

N2 - Contingent upon concentration, reactive oxygen species (ROS) influence cancer evolution in apparently contradictory ways, either initiating/stimulating tumorigenesis and supporting transformation/proliferation of cancer cells or causing cell death. To accommodate high ROS levels, tumor cells modify sulfur-based metabolism, NADPH generation and the activity of antioxidant transcription factors. During initiation, genetic changes enable cell survival under high ROS levels by activating antioxidant transcription factors or increasing NADPH via the pentose phosphate pathway (PPP). During progression and metastasis, tumor cells adapt to oxidative stress by increasing NADPH in various ways, including activation of AMPK, the PPP, and reductive glutamine and folate metabolism.

AB - Contingent upon concentration, reactive oxygen species (ROS) influence cancer evolution in apparently contradictory ways, either initiating/stimulating tumorigenesis and supporting transformation/proliferation of cancer cells or causing cell death. To accommodate high ROS levels, tumor cells modify sulfur-based metabolism, NADPH generation and the activity of antioxidant transcription factors. During initiation, genetic changes enable cell survival under high ROS levels by activating antioxidant transcription factors or increasing NADPH via the pentose phosphate pathway (PPP). During progression and metastasis, tumor cells adapt to oxidative stress by increasing NADPH in various ways, including activation of AMPK, the PPP, and reductive glutamine and folate metabolism.

KW - oxidative stress

KW - reactive oxygen species

KW - adaptation

KW - glutathione

KW - thioredoxin

KW - NADPH generation

KW - pentose phosphate pathway

KW - reductive glutamine metabolism

KW - folate metabolism

KW - redox signaling

KW - antioxidant

KW - NRF2

KW - BACH1

KW - AP-1

KW - FOXO

KW - PGC-1alpha

KW - HIF-1alpha

KW - HSF1

KW - NF-κB

KW - TP53

KW - tumorigenesis

KW - initiation

KW - progression

KW - metastasis

KW - dormant cancer cell

KW - recurrent disease

UR - http://www.scopus.com/inward/record.url?scp=85088396010&partnerID=8YFLogxK

U2 - 10.1016/j.ccell.2020.06.001

DO - 10.1016/j.ccell.2020.06.001

M3 - Review article

C2 - 32649885

SN - 1535-6108

VL - 38

SP - 167

EP - 197

JO - Cancer Cell

JF - Cancer Cell

IS - 2

ER -

Oxidative Stress in Cancer

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

Access to Document

Other files and links

Fingerprint

Defining the Oxidative Stress-Related Mechanisms by which Activation of the Transcription Factor Nrf2 Arrests and Resolves Liver Fibrosis

Contribution by NRF2 Upregulation to Lung Carcinogenesis and the Possible Therapeutic Value of NRF2 Inhibition by GSK-3 (Joint with Universities of St Andrews, Edinburgh and Pennsylvania)

Hayes, John

Cite this

Oxidative Stress in Cancer

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

Access to Document

Other files and links

Fingerprint

Projects

Defining the Oxidative Stress-Related Mechanisms by which Activation of the Transcription Factor Nrf2 Arrests and Resolves Liver Fibrosis

Contribution by NRF2 Upregulation to Lung Carcinogenesis and the Possible Therapeutic Value of NRF2 Inhibition by GSK-3 (Joint with Universities of St Andrews, Edinburgh and Pennsylvania)

Profiles

Hayes, John

Cite this