Abstract
Abstract Prostate cancer is usually androgen-dependent and responds well to androgen ablation therapy. However, at a certain stage some prostate cancers eventually acquire a castration-resistant phenotype. These cancer cells are originally high-grade and show very poor response to any anticancer therapies. To characterize the molecular features of clinical high-grade prostate cancers, we analyzed gene-expression profiles by genome-wide cDNA microarray combined with microdissection and found dozens of trans-activated genes in clinical high-grade prostate cancers. Among them, we report the identification of a new biomarker, KURO3. We confirmed overexpression of KURO3 in high-grade prostate cancer cells by RT-PCR. Knockdown of KURO3 expression by siRNA in a prostate cancer cell line resulted in a drastic decrease of cell numbers. In contrast, KURO3 overexpression in a prostate cancer cell line promoted cell proliferation. These findings suggest that KURO3 could be involved in aggressive phenotype of prostate cancers, including hormone-resistant prostate cancers, and that it should be a potential molecular target for development of new therapeutics and a diagnostic biomarker for aggressive prostate cancers. 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 1675. doi:10.1158/1538-7445.AM2011-1675
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