Abstract

Abstract HDGF was identified as an oncogene relevant for colon cancer carcinogenesis by cDNA-array analysis, RT-PCR and immunohistochemistry. The analysis were performed in colonic adenoma (Geki2), carcinoma (HT29) and metastasis (SW620) cell lines, and in 50 colorectal cancer tissues and corresponding normal mucosa. By incubation of the cell lines with the short chain fatty acid butyrate (4mM), it was possible to (down-) regulate the HDGF-expression level. In the patients we analysed, HDGF overexpression was not associated with a worse prognosis or any other clinical parameter. To study the mechanisms of action of HDGF we stably transfected a HDGF-siRNA containing plasmid into HT29 colon carcinoma cells, resulting in a almost complete inactivation of HDGF-expression. This blocking leads to altered growth characteristics and cell differentiation and the cells exhibit potent pro-apoptotic properties. An affymetrix-expression array was performed and first results will me shown at the meeting. In conclusion, HDGF might be a potential therapeutic target for human colorectal cancer and a modulation of expression is possible by the short chain fatty acid butyrate. These findings may have major implications in the treatment of colorectal cancer. 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 2248. doi:10.1158/1538-7445.AM2011-2248

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