Cancer chemoprevention and mitochondria: targeting apoptosis in transformed cells via the disruption of mitochondrial bioenergetics/redox state.

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.

Cancer chemoprevention: a radical perspective.

Cancer chemopreventive agents block the transformation of normal cells and/or suppress the promotion of premalignant cells to malignant cells. Certain agents may achieve these objectives by modulating xenobiotic biotransformation, protecting cellular elements from oxidative damage, or promoting a more differentiated phenotype in target cells. Conversely, various cancer chemopreventive agents can encourage apoptosis in premalignant and malignant cells in vivo and/or in vitro, which is conceivably another anticancer mechanism.

Mitochondrial reactive oxygen species affect sensitivity to curcumin-induced apoptosis.

Curcumin exhibits anticancer activity in vivo and triggers tumor cell apoptosis in vivo and in vitro. Several in vitro studies suggest that curcumin-induced apoptosis is associated with reactive oxygen species (ROS) production and/or oxidative stress in transformed cells. This study compared and contrasted the effects of curcumin on human skin cancer cells and their respiration-deficient (rho0) clones to characterize the prospective oxidative stress signaling responsible for initiating apoptosis.