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[Cancer Research 64, 423-428, January 1, 2004]
© 2004 American Association for Cancer Research

Endocrinology

Estrogen Receptor ß Inhibits Human Breast Cancer Cell Proliferation and Tumor Formation by Causing a G2 Cell Cycle Arrest

Sreenivasan Paruthiyil13, Hema Parmar23, Vaishali Kerekatte4, Gerald R. Cunha23, Gary L. Firestone4 and Dale C. Leitman13

1Departments of Obstetrics, Gynecology, and Reproductive Sciences, Cellular and Molecular Pharmacology and 2Anatomy, and 3Center for Reproductive Sciences, University of California, San Francisco, and 4Department of Molecular and Cellular Biology, University of California, Berkeley, California

Studies indicate that estrogen receptor (ER) {alpha} mediates breast cancer-promoting effects of estrogens. The role of ERß in breast cancer is unknown. Elucidating the role of ERß in the pathogenesis of breast cancer is important because many human breast tumors express both ER{alpha} and ERß. We show that adenovirus-mediated expression of ERß changes the phenotype of ER{alpha}-positive MCF-7 cells. Estradiol increases cell proliferation and causes tumor formation of MCF-7 cells expressing only ER{alpha}. In contrast, introducing ERß into MCF-7 cells causes an inhibition of proliferation in vitro and prevents tumor formation in a mouse xenograft model in response to estradiol. ERß inhibits proliferation by repressing c-myc, cyclin D1, and cyclin A gene transcription, and increasing the expression of p21Cip1 and p27Kip1, which leads to a G2 cell cycle arrest. These results demonstrate that ER{alpha} and ERß produce opposite effects in MCF-7 cells on cell proliferation and tumor formation. Natural or synthetic ERß-selective estrogens may lack breast cancer promoting properties exhibited by estrogens in hormone replacement regimens and may be useful for chemoprevention of breast cancer.




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