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Carcinogenesis Advance Access originally published online on December 6, 2006
Carcinogenesis 2007 28(2):233-239; doi:10.1093/carcin/bgl243
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© The Author 2006. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Apoptosis by dietary factors: the suicide solution for delaying cancer growth

Naghma Khan, Farrukh Afaq and Hasan Mukhtar*

Department of Dermatology, University of Wisconsin–Madison, Medical Sciences Center B-25, 1300 University Avenue, Madison, WI 53706, USA

*To whom correspondence should be addressed. Tel: +1 608 263 3927; Fax: +1 608 263 5223; Email: hmukhtar{at}wisc.edu

Apoptosis, a form of programmed cell death, plays a fundamental role in the maintenance of tissues and organ systems by providing a controlled cell deletion to balanced cell proliferation. The last decade has witnessed an exponential increase in the number of studies investigating how different components of the diet interact at the molecular and cellular level to determine the fate of a cell. It is now apparent that many dietary chemopreventive agents with promise for human consumption can also preferentially inhibit the growth of tumor cells by targeting one or more signaling intermediates leading to induction of apoptosis. In this brief review, we summarize the available evidence for dietary chemopreventive substances as inducers of apoptosis in cancer cells. These emerging data suggest that some of these dietary agents especially those which humans could be persuaded to consume may be utilized in the prevention and management of cancer.

Abbreviations: Apaf-1, apoptotic protease-activating factor 1; Bid, Bcl-2 interacting domain; c-FLIP, FADD-like interleukin-1ß-converting enzyme inhibitory protein; DIABLO, direct IAP-binding protein with low pI; EGCG, (–)-epigallocatechin gallate; FADD, Fas-associated protein with death domain; IAP, inhibitors of apoptosis protein; MMP, mitochondrial membrane potential; PARP, poly (ADP-ribose) polymerase; Smac, second mitochondria-derived activator of caspase; TNF, tumor necrosis factor; TRAIL, TNF-related apoptosis-inducing ligand; UV, ultraviolet

Received October 11, 2006; revised November 21, 2006; accepted November 27, 2006.


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