Thromb Haemost 1992; 68(06): 662-666
DOI: 10.1055/s-0038-1646340
Original Article
Schattauer GmbH Stuttgart

Expression of Urokinase and Its Receptor in Invasive and Non-Invasive Prostate Cancer Cell Lines

W Hollas
1   The Department of Tumor Biology, M. D. Anderson Cancer Center, Houston, TX, USA
,
N Hoosein
2   The Urology Research Laboratory, M. D. Anderson Cancer Center, Houston, TX, USA
,
L W K Chung
2   The Urology Research Laboratory, M. D. Anderson Cancer Center, Houston, TX, USA
,
A Mazar
3   The Thrombolytics Venture Abbott Labs, Abbott Park, IL, USA
,
J Henkin
3   The Thrombolytics Venture Abbott Labs, Abbott Park, IL, USA
,
K Kariko
4   The Department of Medicine, University of Pennsylvania, Philadelphia, PA, USA
,
E S Barnathan
4   The Department of Medicine, University of Pennsylvania, Philadelphia, PA, USA
,
D Boyd
1   The Department of Tumor Biology, M. D. Anderson Cancer Center, Houston, TX, USA
› Author Affiliations
Further Information

Publication History

Received 21 January 1992

Accepted after revision 03 July 1992

Publication Date:
04 July 2018 (online)

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Summary

We previously reported that extracellular matrix invasion by the prostate cancer cell lines, PC-3 and DU-145 was contingent on endogenous urokinase being bound to a specific cell surface receptor. The present study was undertaken to characterize the expression of both urokinase and its receptor in the non-invasive LNCaP and the invasive PC-3 and DU-145 prostate cells. Northern blotting indicated that the invasive PC-3 cells, which secreted 10 times more urokinase (680 ng/ml per 106 cells per 48 h) than DU-145 cells (63 ng/ml per 106 cells per 48 h), had the most abundant transcript for the plasminogen activator. This, at least, partly reflected a 3 fold amplification of the urokinase gene in the PC-3 cells. In contrast, urokinase-specific transcript could not be detected in the non-invasive LNCaP cells previously characterized as being negative for urokinase protein. Southern blotting indicated that this was not a consequence of deletion of the urokinase gene. Crosslinking of radiolabelled aminoterminal fragment of urokinase to the cell surface indicated the presence of a 51 kDa receptor in extracts of the invasive PC-3 and DU-145 cells but not in extracts of the non-invasive LNCaP cells. The amount of binding protein correlated well with binding capacities calculated by Scatchard analysis. In contrast, the steady state level of urokinase receptor transcript was a poor predictor of receptor display. PC-3 cells, which were equipped with 25,000 receptors per cell had 2.5 fold more steady state transcript than DU-145 cells which displayed 93,000 binding sites per cell.