期刊
EUROPEAN JOURNAL OF CANCER
卷 45, 期 4, 页码 685-693出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.ejca.2008.11.023
关键词
Benign prostatic hyperplasia; Collagen receptor; Endo180; Invasion; Metastasis; Prostate cancer; Proteases
类别
资金
- Hammersmith Hospital Special Trustees
- Tony & Rita Gallagher Fellowship
- Prostate Cancer Charity [110632]
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. (C) 2008 Elsevier Ltd. All rights reserved.
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