Molecular Targets for Nutrients Involved with Cancer Prevention

Abstract

Dietary nutrients can influence cancer risk by inhibiting or enhancing carcinogenesis through diverse mechanisms of action. The identification and elucidation of their sites of action have been a focus of nutrition and cancer research for more than four decades. Transforming nutrition and cancer research from a predominantly observational to a molecular approach offers exciting opportunities for truly identifying those who will and will not benefit from dietary intervention strategies. The emerging field of nutritional genomics, defined here as the study of any genetic or epigenetic interaction with a nutrient, will be key to this evolution. Unraveling which genetic upregulation or downregulation leads to subsequent phenotype changes will not be easy. There is evidence that genetic polymorphisms can influence the dynamics between nutrients and molecular targets and, thus, contribute to variation in response among individuals. Because many molecular targets will likely be identified, it may be necessary to credential nutrients, that is, to determine which specific nutrient-related genetic and epigenetic changes bring about phenotypic changes, to establish which interactions are the most important and under what circumstances. Vitamin D, calcium, folate, selenium, genistein, and resveratrol are highlighted, because they represent specific classes of nutrients and illustrate the need to credential various nutrients to understand their physiological significance in cancer prevention. As the science of nutrition unfolds, a clearer understanding will emerge about how nutrients can modulate cancer risk through molecular interactions and how foods might be changed by agronomic approaches and/or biotechnology. Undeniably, embracing new genomic technologies offers exciting opportunities for advances in the broad area of nutrition, especially those related to cancer prevention.

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“…40,41 Multiple potential mechanisms involving initiation, promotion and progression have been identified. 42,43 Although our observations support an antineoplastic role of resveratrol as reported by Savouret et al, 44 grape intake even among the highest quartiles was very low. It is not known whether intakes at this level could impart protection or whether grape intake is a marker of other dietary behavior.…”

β-Escin inhibits colonic aberrant crypt foci formation in rats and regulates the cell cycle growth by inducing p21waf1/cip1 in colon cancer cells

“…Risk reduction by nutritional intervention holds promise for both prevention and control of colon cancer (2,3); an alternative approach to identify specific chemopreventive agents holds additional promise (4). Evaluation of food-based, naturally occurring phytochemicals and synthetic agents that can reduce the risk and retard or inhibit the development of colon cancer could lead to new strategies for colon cancer chemoprevention.…”

Suppression of Prostate Carcinogenesis by Dietary Supplementation of Celecoxib in Transgenic Adenocarcinoma of the Mouse Prostate Model

“…In the search for agents that will prevent or delay the onset of cancer, it has become apparent that cyclooxygenase (COX)-2 is a promising therapeutic target (1)(2)(3)(4)(5). COX-2 is an inducible isoform of COX, an enzyme that catalyzes the rate-limiting step in prostaglandin synthesis from arachidonic acid (6).…”