Mitochondrial recoupling: a novel therapeutic strategy for cancer?

被引：78
作者：
Baffy, G. [1 ,2 ]
Derdak, Z. [3 ,4 ]
Robson, S. C. [5 ]
机构：
[1] Harvard Univ, Sch Med, VA Boston Healthcare Syst, Dept Med, Boston, MA 02130 USA
[2] Harvard Univ, Sch Med, Brigham & Womens Hosp, Boston, MA 02130 USA
[3] Brown Univ, Rhode Isl Hosp, Liver Res Ctr, Dept Med, Providence, RI 02903 USA
[4] Brown Univ, Alpert Sch Med, Providence, RI 02903 USA
[5] Harvard Univ, Sch Med, Liver Clin, Dept Med,Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA
来源：
BRITISH JOURNAL OF CANCER | 2011年 / 105卷 / 04期
关键词：
uncoupling proteins; UCP2; aerobic glycolysis; metabolic reprogramming; oxidative stress; p53; BETA-CELL DYSFUNCTION; UNCOUPLING PROTEIN-2; PROTON LEAK; P53; SUPEROXIDE; EXPRESSION; OBESITY; GLYCOLYSIS;
D O I：
10.1038/bjc.2011.245
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Recent findings link metabolic transformation of cancer cells to aberrant functions of mitochondrial uncoupling proteins (UCPs). By inducing proton leak, UCPs interfere with mitochondrial synthesis of adenosine 5'-triphosphate, which is also a key determinant of glycolytic pathways. In addition, UCP suppress the generation of superoxide, a byproduct of mitochondrial electron transport and a major source of oxidative stress. The near ubiquitous UCP2 becomes highly abundant in some cancers and may advance metabolic reprogramming, further disrupt tumour suppression, and promote chemoresistance. Here we review current evidence to suggest that inhibition of mitochondrial uncoupling may eliminate these responses and reveal novel anti-cancer strategies. British Journal of Cancer (2011) 105, 469-474. doi: 10.1038/bjc. 2011.245 www.bjcancer.com Published online 28 June 2011 (C) 2011 Cancer Research UK
引用
收藏
页码：469 / 474
页数：6
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