Abstract 2907: Role of reactive oxygen and nitrogen species in resveratrol-induced lung cancer cell death.

Abstract

Abstract Lung cancer is the leading cause of cancer related deaths worldwide. In 2008, 158,592 deaths were attributed to this disease and 208,493 new cases were diagnosed in the United States. Resveratrol (trans-3, 5, 4′-trihydroxystilbene), a compound found largely in the skins of red grapes, has been reported to be a promising anticancer agent in various types of cancer. The primary goal of this study is to delineate the key signaling pathways induced in response to resveratrol leading to lung cancer cell death. In this study, we use non-tumorigenic human bronchial epithelial (BEAS-2B) and human lung epithelial cancer (H460) cells to model the response of lung tissue to resveratrol. We observed an increase in superoxide, hydrogen peroxide and nitric oxide production in response to resveratrol treatment in lung cancer cells (H460) as compared to non-tumorigenic cells (BEAS-2B). Additionally, our data shows an increase in BEAS-2B cell viability as compared to H460 cell viability in response to resveratrol treatment. Overall, we observe an increase in cellular oxidative and nitrosative stress in cancer cells in response to resveratrol treatment which may be responsible for increased apoptosis and decreased viability in these cells. Subsequently, we plan to identify the specific reactive species as well as the major apoptotic pathway induced in response to resveratrol treatment in both normal and cancer cells. We expect resveratrol to have significant effect on lung cancer cells via oxidative/nitrosative stress-mediated modulation of key apoptotic biomarkers. This study will establish the protective role of resveratrol in the pathogenesis of lung cancer and the information can be potentially exploited to improve future lung cancer therapies. Citation Format: Elizabeth S. Monillas, Grayson Walker, Aubrey Brockmiller, Anand Iyer, Neelam Azad. Role of reactive oxygen and nitrogen species in resveratrol-induced lung cancer cell death. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2907. doi:10.1158/1538-7445.AM2013-2907