ROS signaling under metabolic stress: cross-talk between AMPK and AKT pathway

被引：569

作者：

Zhao, Yang ^{[1
]}

Hu, Xingbin ^{[1
]}

Liu, Yajing ^{[1
]}

Dong, Shumin ^{[1
]}

Wen, Zhaowei ^{[1
]}

He, Wanming ^{[1
]}

Zhang, Shuyi ^{[1
]}

Huang, Qiong ^{[1
]}

Shi, Min ^{[1
]}

机构：

[1] Southern Med Univ, Nanfang Hosp, Dept Oncol, Guangzhou, Guangdong, Peoples R China

来源：

MOLECULAR CANCER | 2017年 / 16卷

基金：

中国国家自然科学基金;

关键词：

Reactive oxygen species; Metabolic stress; AMPK; AKT; mTOR; FOXO; ACTIVATED PROTEIN-KINASE; DEPRIVATION-INDUCED CYTOTOXICITY; OXYGEN SPECIES ROS; OXIDATIVE STRESS; GLUCOSE DEPRIVATION; CANCER GROWTH; AEROBIC GLYCOLYSIS; AMPK-FOXO3A AXIS; REDOX REGULATION; ENERGY SENSOR;

D O I：

10.1186/s12943-017-0648-1

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Cancer cells are frequently confronted with metabolic stress in tumor microenvironments due to their rapid growth and limited nutrient supply. Metabolic stress induces cell death through ROS-induced apoptosis. However, cancer cells can adapt to it by altering the metabolic pathways. AMPK and AKT are two primary effectors in response to metabolic stress: AMPK acts as an energy-sensing factor which rewires metabolism and maintains redox balance. AKT broadly promotes energy production in the nutrient abundance milieu, but the role of AKT under metabolic stress is in dispute. Recent studies show that AMPK and AKT display antagonistic roles under metabolic stress. Metabolic stress-induced ROS signaling lies in the hub between metabolic reprogramming and redox homeostasis. Here, we highlight the cross-talk between AMPK and AKT and their regulation on ROS production and elimination, which summarizes the mechanism of cancer cell adaptability under ROS stress and suggests potential options for cancer therapeutics.

引用

页数：12

共 124 条

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