Abstract 4136: Effects of magnolol on cell cycle, STAT 3, NF-kappa B and AKT signaling

Abstract

Abstract Magnolol is plant lignan isolated from bark and seed cones of Magnolia glaucan has been investigated for its anticancer effects. Previous studies from our laboratory have shown magnolol to be chemopreventive against UVB-caused skin carcinogenesis by inducing apoptosis. The objective of present study is to investigate other mechanisms involved for its chemopreventive effects. For this investigation, A431 human epidermoid carcinoma cells were used. Effects of magnolol on cell cycle were determined by flow cytometry. Expressions of various proteins involved in cell cycle were determined by Western blotting using appropriate antibodies. A431 human epidermoid carcinoma cells were incubated with different concentrations at different time periods. We further investigated the effects of magnolol on signal transducer and activator of transcription (STAT 3), nuclear factor-kappa B (NF-kappa B/p65) and AKT signaling pathways that play an important role in cell proliferation and survival. Magnolol at 100 μM and 125 µM caused G0/G1 cell cycle arrest by decreasing cyclin D1, cyclin D2, and CDK 4 and by increasing CDK inhibitors p21 and p27 at 24 and 48 h. We further found that magnolol inhibited expressions of STAT 3, NF-kappa B and AKT by inhibiting their phosphorylation at 24 and 48 h. These results indicate that chemopreventive effects of magnolol are mediated through multiple mechanisms. This study is supported by Translational Cancer Research Center funded as one of the 2010 Research Initiative Center by the State of South Dakota. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4136.