Cancer chemoprevention and mitochondria: Targeting apoptosis in transformed cells via the disruption of mitochondrial bioenergetics/redox state
- 23 December 2008
- journal article
- review article
- Published by Wiley in Molecular Nutrition & Food Research
- Vol. 53 (1), 49-67
- https://doi.org/10.1002/mnfr.200700527
Abstract
Cancer chemoprevention employs agents that block, hinder, or reverse tumorigenesis to prevent malignancy. Several putative cancer chemopreventive agents promote apoptosis in transformed cells initiated in animal carcinogenesis models or identified in human subjects, and/or in tumor cells cultured in vitro. Consequently, apoptosis induction is increasingly valued as a biologically significant anticancer mechanism in the arena of chemoprevention. In vitro studies suggest that the permeabilization of mitochondrial membranes is an important mechanistic determinant associated with the apoptosis induced by these agents. Mitochondrial membrane permeabilization (MMP) may occur via the control of proapoptotic Bcl‐2 family members, and/or by the induction of the mitochondrial permeability transition. Both of these cell death‐inducing regulatory mechanisms are ultimately responsive to the bioenergetic status/redox state of mitochondria. Interestingly, in addition to inducing MMP, various chemopreventive agents can directly modulate mitochondrial bioenergetics and/or redox tone in transformed cells. This review will examine prospective mechanisms associated with the disruption of mitochondrial function by chemopreventive agents that affect MMP and apoptosis. In doing so, we will construct a paradigm supporting the notion that the bioenergetic and/or redox characteristics of the mitochondria in transformed cells are important targets in the chemoprevention of cancer.Keywords
This publication has 167 references indexed in Scilit:
- Vanilloid receptor agonists and antagonists are mitochondrial inhibitors: How vanilloids cause non-vanilloid receptor mediated cell deathBiochemical and Biophysical Research Communications, 2007
- Role of epigallocatechin gallate (EGCG) in the treatment of breast and prostate cancerLife Sciences, 2006
- Molecular mechanism of ‘mitocan’‐induced apoptosis in cancer cells epitomizes the multiple roles of reactive oxygen species and Bcl‐2 family proteinsFEBS Letters, 2006
- Curcumin: The story so farEuropean Journal Of Cancer, 2005
- ROS stress in cancer cells and therapeutic implicationsDrug Resistance Updates, 2004
- Deguelin inhibits the growth of colon cancer cells through the induction of apoptosis and cell cycle arrestEuropean Journal Of Cancer, 2002
- Hypoxia — a key regulatory factor in tumour growthNature Reviews Cancer, 2002
- Involvement of Caspase-3 in Epigallocatechin-3-gallate-Mediated Apoptosis of Human Chondrosarcoma CellsBiochemical and Biophysical Research Communications, 2000
- Synthetic retinoid CD437 promotes rapid apoptosis in malignant human epidermal keratinocytes and G1 arrest in their normal counterpartsJournal of Cellular Physiology, 2000
- The mitochondrial permeability transitionBiochimica et Biophysica Acta (BBA) - Reviews on Biomembranes, 1995