Abstract 1167: The expression of urokinase plasminogen activator (uPA) system genes in prostate carcinoma is related to clinicopathological parameters

Abstract

Abstract Background: Prostate cancer (PCa) is a leading cause of tumor mortality. Members of the urokinase plasminogen activator (uPA) system play an important role in tumorigenesis in many human malignancies. We sought to characterize the mRNA expression of uPA members in primary PCa samples and to correlate this expression to clinicopathological parameters. Material and methods: We investigated the mRNA expression level of three members of the uPA system (uPA, PAI-1 and uPAR) using 26 paired samples of PCa and adjacent non-malignant tissue. Absolute quantification of gene expression was performed by quantitative PCR and subsequent standardization on the reference gene TBP. Gene expression measures were further correlated to clinicopathological characteristics as TNM classification, Gleason sum, and tumor grade. Results: Although we did not detect significant differences in expression of uPA system genes between tumor and matched nonmalingnant tissue in our patient cohort, we identified a positive correlation of all three uPA family members (p<0.01; bivariate correlation). When stratifying PAI-1 expression according to the median mRNA level we discovered correlations to defined tumor characteristics. Tumors with PAI-1 expression above median displayed a higher Gleason sum (8 or 9) than tumors expressing less-than-median PAI-1 (p=0.03, Fisher's exact test). Likewise, an elevated PAI-1 expression was correlated with higher tumor grade (p=0.01; Fisher exact test) and tumor stage (p=0.046; Fisher exact test). Conclusion: Our results demonstrate that mRNA expression of PAI-1 as a member of the uPA family correlates with characteristic pathological parameters of PCa. 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 1167. doi:1538-7445.AM2012-1167