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Estrogen Receptor- in the Inhibition of Cancer Growth and Angiogenesis

Department of Biochemistry, Roswell Park Cancer Institute [S. H. A.], State University of New York at Buffalo [S. H. A., A. L. O., D. B., M. B. P., M. J. S., P. D.], Buffalo, New York; Departments of Medicine and Endocrinology [A. L. O.] and Pathology [D. B., M. B. P., M. J. S.], Veterans Administration Medical Center, Buffalo, New York; General Pharmacology, DuPont Pharmaceuticals Company, Wilmington, Delaware 19880-0400 [S. Mou., S. Moh.]; and Endocrine Division, Kaleida Health, Buffalo, New York [S. H. A., P. D.]

A high level of estrogen receptor- (ER-) is believed to be favorable in the prognosis and treatment of certain female cancers. ER- expression in the ER-negative breast cancer cell lines inhibits their proliferation and invasive, metastatic potential in vitro. We stably overexpressed the ER- in the human endometrial cancer cell line Ishikawa and showed that, unlike estradiol, high levels of ER- significantly inhibit the growth of tumors xenografted from the Ishikawa cells. Subsequent to ER- overexpression, in vivo down-regulation of vascular endothelial growth factor was observed in tumor xenografts. In addition, these tumors showed an inhibition of vascularization and of the angiogenic agent, integrin _vß₃. Involvement of a switch in the angiogenic pathways during tumorigenesis has been a recent focus of interest. Our results indicate that a high level of ER- may be beneficial in the control of female cancers because of its inhibitory effect on such angiogenic pathways.

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