Preferential killing of cancer cells with mitochondrial dysfunction by natural compounds

被引:75
作者
Chen, Gang [1 ]
Wang, Feng [1 ,2 ]
Trachootham, Dunyaporn [1 ,3 ]
Huang, Peng [1 ]
机构
[1] Univ Texas MD Anderson Canc Ctr, Dept Mol Pathol, Houston, TX 77030 USA
[2] Univ Texas Houston, Grad Sch Biomed Sci Houston, Houston, TX USA
[3] Thammasat Univ, Fac Dent, Pathum Thani, Thailand
基金
美国国家卫生研究院;
关键词
Mitochondrial dysfunction; Energy metabolism; Reactive oxygen species; Apoptosis; 2 Phenethyl isothiocyanate; Honokiol; VITAMIN-E ANALOGS; RESVERATROL INDUCES APOPTOSIS; HONOKIOL-INDUCED APOPTOSIS; HUMAN LEUKEMIA-CELLS; OSW SAPONIN ANALOGS; DRINKING GREEN TEA; PHASE-I TRIAL; OXIDATIVE STRESS; PHENETHYL ISOTHIOCYANATE; ANTICANCER AGENTS;
D O I
10.1016/j.mito.2010.08.001
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Mitochondria play essential roles in cellular metabolism redox homeostasis and regulation of cell death Emerging evidences suggest that cancer cells exhibit various degrees of mitochondrial dysfunctions and metabolic alterations which may serve as a basis to develop therapeutic strategies to preferentially kill the malignant cells Mitochondria as a therapeutic target for cancer treatment is gaining much attention in the recent years and agents that impact mitochondria with anticancer activity have been identified and tested in vitro and in vivo using various experimental systems Anticancer agents that directly target mitochondria or indirectly affect mitochondrial functions are collectively classified as mitocans This review article focuses on several natural compounds that preferentially kill cancer cells with mitochondrial dysfunction and discusses the possible underlying mechanisms and their therapeutic implications in cancer treatment Mitocans that have been comprehensively reviewed recently are not included in this article Important issues such as therapeutic selectivity and the relevant biochemical basis are discussed in the context of future perspectives (C) 2010 Elsevier BV and Mitochondria Research Society All rights reserved
引用
收藏
页码:614 / 625
页数:12
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