Abstract 5058: Effects of honokiol on UACC-62 malignant melanoma cell line

Abstract

Abstract Studies from our laboratory have indicated the chemopreventive effects of honokiol on UVB-induced squamous cell carcinoma in mouse skin. The purpose of this study is to investigate the effects of honokiol on UACC-62 malignant melanoma cell and elucidate the mechanisms of action. UACC-62 cells were grown in RPMI media in cell culture conditions. The effects of honokiol on cell viability and cell proliferation were studied by the MTT and BrdU assays. To investigate the effects of honokiol on cell cycle, UACC-62 cells were treated with honokiol, stained with propidium iodide and analyzed by flow cytometry. Cell lysates were prepared in similar conditions as the previous experiments to assess how honokiol affected the expressions of proteins involved in different pathways. The MTT assay showed a significant decrease in cell viability starting at 75 μM honokiol at 24 hours. The BrdU assay results indicated decreased cell proliferation as early as 12 hours and 50 μM honokiol. The cell cycle analysis indicated that honokiol caused G0/G1 phase arrest in melanoma cells (p < 0.05) at 24h and 50 μM. Western blots of the cell lysates prepared showed that honokiol decreased the expressions of cyclin E, CDK4, cyclin D2, NF-kβ, and p-MEK starting at 50 μM honokiol at 24 hours. The expressions of apoptotic proteins cleaved caspase-3, cleaved caspase-9, caspase 8, and cleaved PARP were increased by honokiol treatments. This data indicated that honokiol decreases cell proliferation and induces apoptosis of UACC-62 cells thus could be a candidate for pre-clinical studies as an agent for treating or preventing melanoma skin cancer. Supported by Translational Cancer Research Center funded as a 2010 Research Initiative Center by the State of South Dakota. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 5058. doi:10.1158/1538-7445.AM2011-5058