Abstract
Abstract Several classes of natural products have cancer prevention potential and PPAR gamma is an intriguing chemoprevention target as a nuclear receptor that controls multiple growth and differentiation processes. We have previously tested many classes of natural products in A/J mice and have found that the following chemoprevention compounds had no significant dietary toxicities: inositol, eucalyptol, chalcones, nicotinamides, and resveratrol. We tested these compounds for their capacity to activate PPAR gamma reporter genes in CA-9-22 oral cancer cells. In several repeated experiments we found that Inositol hexaphosphate did not activate PPAR gamma reporter genes at high concentrations of 1-4 mM. We found that eucalyptol, trans-Chalcone, 4 methoxy chalcone, Nicotinic Acid, and Nicotinamide had the capacity for statistically significant activation of PPAR gamma reporter genes in oral cancer cells from 20-60% at concentrations of 1-100 uM. We found that resveratrol was the most potent agent and could activate PPAR gamma reporter genes 2 fold. As a reference, this was about half the activity of the prototypic PPAR gamma activator pioglitazone. We performed additional experiments with resveratrol and found that it could activate the PPAR gamma dependent squamous differentiation gene Involucrin in oral cancer cells and BEAS 2B cells. Additionally, resveratrol significantly decreased BEAS 2 B proliferation from 48-96 hours at concentrations of 10 uM. From this data we conclude that resveratrol has the capacity to activate PPAR gamma in vitro and resveratrol and its derivatives may also function as PPAR gamma activators as an additional mechanism of action. We also conclude that inositol, eucalyptol, chalcones, and nicotinamides do not activate PPAR gamma. Citation Format: Jennifer Diaz, Beverly Wuertz, Art Galbraith, Frank G. Ondrey. Effects of chalcones, nicotinamide, and resveratrol on PPAR gamma activation in oral cancer cells. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2611.
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