Abstract 4623: Capsaicin represses transcriptional activity of β-catenin in human colorectal cancer cells

Abstract

Abstract Capsaicin is a pungent ingredient in chili red peppers and has been linked to suppression of growth in various cancer cells. However, the underlying mechanism(s) by which capsaicin induces growth arrest and apoptosis of cancer cells is not completely understood. In the present study, we investigated whether capsaicin alters β-catenin signaling in human colorectal cancer cells in vitro. Exposure of human colorectal cancer cells to capsaicin suppressed cell proliferation. Transient transfection with β-catenin responsive reporter gene indicated that capsaicin suppressed transcriptional activity of β-catenin. Capsaicin treatment resulted in a decrease of intracellular β-catenin levels and a reduction of β-catenin transcripts. These results were confirmed by a reduced luciferase reporter activity driven by β-catenin promoter. In addition, capsaicin destabilized β-catenin through enhancement of proteosomal-dependent degradation. Western blot and immunoprecipitation studies indicated that capsaicin treatment disrupted interaction of TCF-4 and β-catenin and suppressed TCF-4 expression. This study identifies an important capsaicin-mediated pathway that contributes to anti-cancer activity of human colorectal cancer cells. 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 4623. doi:10.1158/1538-7445.AM2011-4623