CRANBERRY + GRAPE SEED EXTRACT Cranberry and Grape Seed Extracts Inhibit the Proliferative Phenotype of Oral Squamous Cell Carcinomas
Kourt Chatelain, Spencer Phippen, Jonathan McCabe, Christopher A. Teeters, Susan O’Malley* and Karl Kingsley* Department of Biomedical Sciences, School of Dental Medicine, University of Nevada, Las Vegas, USA
Proanthocyanidins, compounds highly concentrated in dietary fruits, such as cranberries and grapes, demonstrate significant cancer prevention potential against many types of cancer. The objective of this study was to evaluate cranberry and grapeseed extracts to quantitate and compare their anti-proliferative effects on the most common type of oralcancer, oral squamous cell carcinoma. Using two well-characterized oral squamous cell carcinoma cell lines, CAL27 and SCC25, assays were performed to evaluate the effects of cranberry and grape seed extract on phenotypic behaviors of these oralcancers. The proliferation of both oralcancer cell lines was significantly inhibited by the administration of cranberry and grape seed extracts, in a dose-dependent manner. In addition, key regulators of apoptosis,caspase-2 and caspase-8, were concomitantly up-regulated by these treatments. However, cranberry and grape seed extracts elicited differential effects on cell adhesion, cell morphology,and cell cycle regulatory pathways. This study represents one of the first comparative investigations of cranberry and grapeseed extracts and their anti-proliferative effects on oralcancers.Previous findings using purified proanthocyanidin from grapeseed extract demonstrated more prominent growth inhibition,as well as apoptosis-inducing, properties on CAL27 cells. These observations provide evidence that cranberry and grape seed extracts not only inhibit oralcancerproliferation but also that the mechanism of this inhibition may function by triggering key apoptotic regulators in these cell lines. This informationwill be of benefit to researchers interested in elucidating which dietary components are central to mechanisms involved in the mediation oforal carcinogenesis and progression.