Abstract 1849: Identification and functional analysis of SHISA2 overexpressed in prostate cancer
Abstract Prostate cancer (PC) 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 anticance...
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Published in | Cancer research (Chicago, Ill.) Vol. 72; no. 8_Supplement; p. 1849 |
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Main Authors | , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
15.04.2012
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Online Access | Get full text |
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Summary: | Abstract
Prostate cancer (PC) 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 identify novel molecular cancer drug targets, we previously analyzed the gene expression profiles of high-grade PCs using a cDNA microarray combined with laser microbeam microdissection and found a number of genes that are transactivated in high-grade PC. Among them, we report the identification of a novel molecular target, SHISA2. We confirmed overexpression of SHISA2 in high-grade prostate cancer cells by semi-quantitative RT-PCR and immunohistochemical analysis. Knockdown of SHISA2 expression by siRNA in a prostate cancer cell line resulted in a drastic decrease of cell numbers. In contrast, SHISA2 overexpression in a prostate cancer cell line promoted cell proliferation. These findings suggest that SHISA2 could be involved in aggressive phenotype of prostate cancers, including castration-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 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1849. doi:1538-7445.AM2012-1849 |
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ISSN: | 0008-5472 1538-7445 |
DOI: | 10.1158/1538-7445.AM2012-1849 |