Uncoupling protein-2 and cancer

被引：99

作者：

Baffy, Gyorgy ^{[1
,2
]}

机构：

[1] Harvard Univ, Sch Med, VA Boston Healthcare Syst, Boston, MA 02115 USA

[2] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA

来源：

MITOCHONDRION | 2010年 / 10卷 / 03期

关键词：

Cancer; Warburg effect; Metabolic reprogramming; Uncoupling protein-2; Oxidative stress; Chemoresistance; HYPOXIA-INDUCIBLE FACTOR-1; MITOCHONDRIAL PROTON LEAK; BETA-CELL DYSFUNCTION; SKELETAL-MUSCLE UCP2; BROWN ADIPOSE-TISSUE; KAPPA-B ACTIVATION; OXIDATIVE STRESS; GENE-EXPRESSION; NITRIC-OXIDE; NONALCOHOLIC STEATOHEPATITIS;

D O I：

10.1016/j.mito.2009.12.143

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Cancer cells respond to unfavorable microenvironments such as nutrient limitation, hypoxia, oxidative stress, and host defense by comprehensive metabolic reprogramming. Mitochondria are linked to this complex adaptive response and emerging evidence indicates that uncoupling protein-2 (UCP2), a mitochondria' inner membrane anion carrier, may contribute to this process. Effects of UCP2 on mitochondrial bioenergetics, redox homeostasis, and oxidant production in cancer cells may modulate molecular pathways of macromolecular biosynthesis, antioxidant defense, apoptosis, cell growth and proliferation, enhancing robustness and promoting chemoresistance. Elucidation of these interactions may identify novel anti-cancer strategies. Published by Elsevier B.V. on behalf of Mitochondria Research Society.

引用

页码：243 / 252

页数：10

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