NRF2-dependent stress defense in tumor antioxidant control and immune evasion

被引：28

作者：

Angeli, Jose Pedro Friedmann ^{[1
]}

Meierjohann, Svenja ^{[2
,3
]}

机构：

[1] Univ Wurzburg, Rudolf Virchow Ctr Integrat & Translat Bioimaging, Wurzburg, Germany

[2] Univ Wurzburg, Inst Pathol, Wurzburg, Germany

[3] Univ Wurzburg, Comprehens Canc Ctr Mainfranken, Wurzburg, Germany

来源：

PIGMENT CELL & MELANOMA RESEARCH | 2021年 / 34卷 / 02期

关键词：

immune evasion; KEAP1; Nrf2; oxidative stress; H2O2-INDUCED OXIDATIVE STRESS; TRANSCRIPTION FACTOR NRF2; CUL3-BASED E3 LIGASE; SMALL MAF PROTEINS; THERAPEUTIC RESISTANCE; HYDROGEN-PEROXIDE; REACTIVE OXYGEN; MELANOMA; ACTIVATION; GENE;

D O I：

10.1111/pcmr.12946

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The transcription factor NRF2 is known as the master regulator of the oxidative stress response. Tumor entities presenting oncogenic activation of NRF2, such as lung adenocarcinoma, are associated with drug resistance, and accumulating evidence demonstrates its involvement in immune evasion. In other cancer types, the KEAP1/NRF2 pathway is not commonly mutated, but NRF2 is activated by other means such as radiation, oncogenic activity, cytokines, or other pro-oxidant triggers characteristic of the tumor niche. The obvious effect of stress-activated NRF2 is the protection from oxidative or electrophilic damage and the adaptation of the tumor metabolism to changing conditions. However, data from melanoma also reveal a role of NRF2 in modulating differentiation and suppressing anti-tumor immunity. This review summarizes the function of NRF2 in this tumor entity and discusses the implications for current tumor therapies.

引用

页码：268 / 279

页数：12

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