Chemoprevention involves the administration of chemical agents to prevent initiation, promotion, and /or progression that occurs during neoplastic development. Magnolol, a plant lignan, isolated from the bark and seed cones of Magnolia glaucan, has been shown to have chemopreventive effects on chemically-induced skin cancer development. The purpose of this investigation is to study chemopreventive effects of magnolol on UV-B induced skin tumor development in SKH-1 mice, a model relevant to humans, and determine possible mechanism of action. Female SKH-1 mice were divided into two groups. Group 1 received acetone (0.2 ml, topical) one hour before UV-B treatment; Group 2 received magnolol (0.2 ml, 30 µg in acetone, topical) before UV-B treatment. Carcinogenesis was induced by UV-B radiations (30 mJ/cm2 /day, 5 days a week) for 30 weeks. Tumor counts and group weights were taken weekly. In vitro studies in human epidermoid A431 cells were carried out to elucidate possible mechanism of action. Magnolol treatment resulted in 40% reduction in tumor multiplicity as compared to control group. Mechanistic studies involving both in vivo and in vitro have shown a possible involvement of caspase-3 and 8, PARP, and p53 activation (P<0.05) leading to the induction of apoptosis and DNA fragmentation. MTT (IC50 is 100 \#956;M), BrdU (IC50 is75 \#956;M) and COX expression assays indicated significant (P<0.05) decreasing effects of magnolol on cell proliferation. Magnolol prevents UV-B induced skin cancer development possibly by decreasing cell proliferation and activating proapoptotic proteins

Citation Information: In: Proc Am Assoc Cancer Res; 2009 Apr 18-22; Denver, CO. Philadelphia (PA): AACR; 2009. Abstract nr 923.

100th AACR Annual Meeting-- Apr 18-22, 2009; Denver, CO