Oxygen availability and metabolic reprogramming in cancer

被引:141
作者
Xie, Hong [1 ,2 ]
Simon, M. Celeste [1 ,3 ]
机构
[1] Univ Penn, Perelman Sch Med, Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA
[2] Univ Penn, Perelman Sch Med, Dept Canc Biol, Philadelphia, PA 19104 USA
[3] Univ Pennsylvania, Perelman Sch Med, Cell & Dev Biol, Philadelphia, PA 19104 USA
基金
美国国家卫生研究院;
关键词
cancer; glucose; glutamine; hypoxia; lipid metabolism; metabolism; IDH; ROS; MITOCHONDRIAL-COMPLEX-III; RENAL-CELL CARCINOMA; ACETYL-COA SYNTHETASE; PYRUVATE-KINASE M2; INDUCIBLE FACTOR-I; GLUTAMINE-METABOLISM; LIPID STORAGE; GLYCOGEN-METABOLISM; TUMOR-GROWTH; DESATURASE;
D O I
10.1074/jbc.R117.799973
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
Hypoxia and dysregulated metabolism are defining features of solid tumors. How cancer cells adapt to low O-2 has been illuminated by numerous studies, with reprogrammed metabolism being one of the most important mechanisms. This metabolic reprogramming not only promotes cancer cell plasticity, but also provides novel insights for treatment strategies. As the most studied O-2 sensor, hypoxia-inducible factor (HIF) is regarded as an important regulator of hypoxia-induced transcriptional responses. This minireview will summarize our current understanding of hypoxia-induced changes in cancer cell metabolism, with an initial focus on HIF-mediated effects, and will highlight how these metabolic alterations affect malignant phenotypes.
引用
收藏
页码:16825 / 16832
页数:8
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