Endo180 expression with cofunctional partners MT1-MMP and uPAR–uPA is correlated with prostate cancer progression

Endo180 (CD280; MRC2; uPARAP) regulates collagen remodelling and chemotactic cell migration through cooperation with membrane type-1 matrix metalloproteinase (MT1-MMP), urokinase-type plasminogen activator receptor (uPAR) and urokinase-type plasminogen activator (uPA). One hundred and sixty nine prostate tissue sections clinically graded as benign prostatic hyperplasia (BPH) (n = 29) or prostate cancer (PCA) with Gleason scores indicating low (⩽7(3 + 4); n = 26), intermediate (7(4 + 3)–8; n = 96) or high (9–10; n = 19) clinical risk were immunofluorescently stained for Endo180, pan-cytokeratin (pCk), vimentin, MT1-MMP and uPAR–uPA. Quantification of % Endo180+/pCk– and Endo180+/pCk+ cells in entire tissue cores revealed stromal (p = 0.0001) and epithelial (p = 0.0001) upregulation of Endo180 in PCA compared to BPH. Epithelial Endo180 expression was significantly different between the three clinical risk groups of PCA (p < 0.05). Correlations with MT1-MMP and uPAR–uPA confirmed the functionality of Endo180 during PCA progression. This molecular evaluation is the first step in the exploration of Endo180 in PCA diagnosis and therapy.