Oxidative Stress in Cancer

被引：1753

作者：

Hayes, John D. ^{[1
]}

Dinkova-Kostova, Albena T. ^{[1
,2
,3
]}

Tew, Kenneth D. ^{[4
]}

机构：

[1] Univ Dundee, Ninewells Hosp & Med Sch, Jacqui Wood Canc Ctr, Div Cellular Med, Dundee DD1 9SY, Scotland

[2] Johns Hopkins Univ, Sch Med, Dept Pharmacol & Mol Sci, Baltimore, MD 21205 USA

[3] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA

[4] Med Univ South Carolina, Dept Cell & Mol Pharmacol, Charleston, SC 29425 USA

来源：

CANCER CELL | 2020年 / 38卷 / 02期

基金：

英国医学研究理事会;

关键词：

NF-KAPPA-B; PENTOSE-PHOSPHATE PATHWAY; REGULATORY T-CELLS; DOUBLE-EDGED-SWORD; NRF2; ACTIVATION; HEPATOCELLULAR-CARCINOMA; HYDROGEN-PEROXIDE; REDOX HOMEOSTASIS; REDUCTIVE CARBOXYLATION; MESENCHYMAL TRANSITION;

D O I：

10.1016/j.ccell.2020.06.001

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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.

引用

页码：167 / 197

页数：31

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