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Eur J Cancer. 2009 Mar;45(4):685-93. doi: 10.1016/j.ejca.2008.11.023. Epub 2008 Dec 26.

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

Author information

1
Prostate Cancer Research Group, Department of Oncology, Division of Surgery, Oncology, Reproductive Biology and Anaesthesia, Faculty of Medicine, Imperial College London, Hammersmith Hospital Campus, Du Cane Road, London W12 0NN, UK.

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 (< or =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.

PMID:
19112015
DOI:
10.1016/j.ejca.2008.11.023
[Indexed for MEDLINE]

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