Abstract 551: Protein biomarkers of human prostate cancer stromal cells

Abstract

Abstract In situ human prostate tumors are not lethal unless they become invasive and metastatic. For cells to become invasive, the prostate gland must undergo disruption of the basal cell layer and degradation of the basement membrane underneath the luminal epithelial cell layer. Although the roles of proteinases in breaking down the basement membrane have been well-studied, little is known about the factors that induce basal cell layer disruption, degeneration, and its eventual disappearance in invasive cancer. It is hypothesized that microenvironmental factors may affect the degradation of the basal cell layer which if protected may prevent tumor progression and invasion. In this study, we have revealed differential protein expression patterns between cells separated from different prostate pathologies and identified several important stromal proteins that may contribute to inflammation and malignant transformation of benign prostate tissues to cancerous tissues using mass spectrometry and proteomics methods. The identifications of these proteins may generate new strategies for the prevention of basal cell layer disruption leading to the eventual blockade of invasive prostate carcinomas. Furthermore, human matrix metalloproteinase-26/endometase/matrilysin-2 was also investigated and its expression in preinvasive human prostate cancer cells may be associated with the expression of some apoptotic markers. This work may contribute to our understanding of epithelial-stromal interaction in the progression of human prostate cancer. (This work was supported in part by grants DAMD17-02-1-0238 and W81XWH-07-1-0225 from DOD, US Congressionally Directed Medical Research Programs, a grant from the Elsa U. Pardee Foundation, and grants from Florida State University to Dr. Q.-X. Sang) Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 551.