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Diet, Autophagy, and Cancer: A Review

¹ Department of Food Science and Human Nutrition, University of Illinois, Urbana, Illinois and ² Nutritional Science Research Group, Division of Cancer Prevention, National Cancer Institute, Bethesda, Maryland

Requests for reprints: Keith Singletary, Department of Food science and Human Nutrition, University of Illinois, 905 South Goodwin Avenue, Urbana, IL 61801. Phone: 217-244-4497; Fax: 217-265-0925. E-mail: kws{at}illinois.edu

A host of dietary factors can influence various cellular processes and thereby potentially influence overall cancer risk and tumor behavior. In many cases, these factors suppress cancer by stimulating programmed cell death. However, death not only can follow the well-characterized type I apoptotic pathway but also can proceed by nonapoptotic modes such as type II (macroautophagy-related) and type III (necrosis) or combinations thereof. In contrast to apoptosis, the induction of macroautophagy may contribute to either the survival or death of cells in response to a stressor. This review highlights current knowledge and gaps in our understanding of the interactions among bioactive food constituents, autophagy, and cancer. Whereas a variety of food components including vitamin D, selenium, curcumin, resveratrol, and genistein have been shown to stimulate autophagy vacuolization, it is often difficult to determine if this is a protumorigenic or antitumorigenic response. Additional studies are needed to examine dose and duration of exposures and tissue specificity in response to bioactive food components in transgenic and knockout models to resolve the physiologic implications of early changes in the autophagy process. (Cancer Epidemiol Biomarkers Prev 2008;17(7):1596–610)