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

Kogianni, Giolanta; Walker, Marjorie M.; Waxman, Jonathan; Sturge, Justin

Authors

Giolanta Kogianni

Marjorie M. Walker

Jonathan Waxman



Abstract

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. © 2008 Elsevier Ltd. All rights reserved.

Journal Article Type Article
Publication Date Mar 1, 2009
Journal European Journal Of Cancer
Print ISSN 1879-0852
Publisher Elsevier
Peer Reviewed Peer Reviewed
Volume 45
Issue 4
Pages 685-693
APA6 Citation Kogianni, G., Walker, M. M., Waxman, J., & Sturge, J. (2009). Endo180 expression with cofunctional partners MT1-MMP and uPAR-uPA is correlated with prostate cancer progression. European Journal of Cancer, 45(4), 685-693. https://doi.org/10.1016/j.ejca.2008.11.023
DOI https://doi.org/10.1016/j.ejca.2008.11.023
Keywords Benign prostatic hyperplasia, Collagen receptor, Endo180, Invasion, Metastasis, Prostate cancer, Proteases,
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