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[Cancer Research 56, 663-668, February 15, 1996]
© 1996 American Association for Cancer Research
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Endothelin-1 Production and Decreased Endothelin B Receptor Expression in Advanced Prostate Cancer1

Joel B. Nelson2, Kirk Chan-Tack, Sean P. Hedican, Scott R. Magnuson, Terry J. Opgenorth, G. Steven Bova and Jonathan W. Simons

James Buchanan Brady Urological Institute Research Laboratories [J. B. N., K. C-T., S. P. H., G. S. B., J. W. S.], Department of Pathology [G. S. B.], and Johns Hopkins Oncology Center [J. W. S.], Johns Hopkins Hospital, Baltimore, Maryland 21287-2411, and Abbott Laboratories, Abbott Park, Illinois 60064-3500 [S. R. M., T. J. O.]

The potent vasoconstrictor endothelin-1 (ET-1) is at its highest concentration in the normal human ejaculate and is associated with the progression of metastatic prostate cancer. ET-1 protein expression is detected in situ in 14 of 14 primary cancers and 14 of 16 metastatic sites of human prostatic carcinoma. Exogenous ET-1 induces prostate cancer proliferation directly and enhances the mitogenic effects of insulin-like growth factor I, insulin-like growth factor II, platelet-derived growth factor, basic fibroblast growth factor, and epidermal growth factor in serum-free conditions in vitro. The ETA-selective receptor antagonist A-127722 inhibits ET-1-stimulated growth, but the ETB-selective receptor antagonist BQ-788 does not. ET-3, an ETB-selective agonist, also had no effect on prostate cancer growth. No specific ETB-binding sites could be demonstrated in any established human prostate cancer cell line tested, and ETB mRNA, detected by reverse transcription PCR, was reduced. The predominance of ETB binding on human benign prostatic epithelial tissue is not present in metastatic prostate cancer by autoradiography. In human prostate cancer progression to metastases, ET-1 and ETA expression are retained, whereas ETB receptor expression is reduced.

1 This work was supported by grants from the American Foundation for Urological Disease, Inc. (to J. B. N., the Dornier Scholar, and K. C-T.) and the Southern Medical Association (to K. C-T.) and by NIH Prostate Cancer SPORE Grant CA-58236.

2 To whom reprint requests should be addressed, at James Buchanan Brady Urological Institute, Marburg 1, Johns Hopkins Hospital, 600 North Wolfe Street, Baltimore, MD 21287-2411.

Received 11/ 1/95. Accepted 1/ 2/96.




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