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The Journal of Clinical Endocrinology & Metabolism Vol. 82, No. 11 3692-3699
Copyright © 1997 by The Endocrine Society

Original Studies

Coexpression and Cross-Regulation of the Prolactin Receptor and Sex Steroid Hormone Receptors in Breast Cancer1

Christopher J. Ormandy2, Rosemary E. Hall, David L. Manning, John F. R. Robertson, Roger W. Blamey, Paul A. Kelly, Robert I. Nicholson and Robert L. Sutherland

Cancer Research Program, Garvan Institute of Medical Research, St. Vincent’s Hospital, Sydney, New South Wales 2010, Australia; Breast Cancer Laboratory, Tenovus Cancer Research Center, University of Wales College of Medicine (D.L.M., R.I.N.), Cardiff CF-4XX, Wales, United Kingdom; the Department of Surgery, City Hospital (J.F.R.R., R.W.B.), Nottingham, United Kingdom NG5 1PB; and INSERM U-344 Endocrinologie Moléculaire, Faculté de Médecine Necker-Enfants Malades (P.A.K.), 75743 Paris Cédex 15, France

Address all correspondence and requests for reprints to: Dr. C. J. Ormandy, Cancer Research Program, Garvan Institute of Medical Research, St. Vincent’s Hospital, Sydney, New South Wales 2010, Australia. E-mail: c.ormandy{at}garvan.unsw.edu.au

The sex steroid hormones and PRL interact synergistically to control the neoplastic growth of the mammary gland. The basis for this hormonal synergy is unknown, but may involve cellular coexpression of the sex steroid and PRL receptors, coupled with receptor cross-regulation. To examine this hypothesis the expression of the sex steroid and PRL receptors was examined in 20 human breast cancer cell lines and 123 primary breast cancers. Regulation of sex steroid receptors by PRL and of the PRL receptor by sex steroids was examined in T-47D and MCF-7 breast cancer cells. Northern analysis of the breast cancer cell lines and tumors indicated that the PRL receptor and the sex steroid receptors were coexpressed. The level of PRL receptor expression in the breast cancer cell lines was linearly related to that of the estrogen and progesterone receptors, but not to that of the androgen receptor. In MCF-7 and T-47D cells, acute treatment with progestins and androgens and long term treatment with estrogens increased PRL receptor levels. Analysis of sex steroid receptor messenger ribonucleic acid and binding activity showed that acute PRL treatment produced a time- and concentration-dependent increase in progesterone receptor and a decrease in androgen receptor. These results indicate that receptors for sex steroids and PRL are coexpressed and are cross-regulated, providing a potential mechanism for the observed synergy among estrogen, progesterone, and PRL in the control of tumor growth.




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