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Papers In Press, published online ahead of print May 1, 2002
J. Biol. Chem, 10.1074/jbc.M201829200
Submitted on February 23, 2002
Revised on April 30, 2002
Accepted on May 1, 2002

Opposing action of estrogen receptors a and b on cyclin D1 gene expression

Meng-Min Liu, Chris Albanese, Carol M. Anderson, Kristin Hilty, Paul Webb, Rosalie M. Uht, Richard H. Price Jr, Richard G. Pestell, and Peter J. Kushner

Department of Medicine, University of California, San Francisco, CA 94112-1640

Corresponding Author: kushner{at}itsa.ucsf.edu

Induction of cyclin D1 gene transcription by estrogen receptor alpha (ERa) plays an important role in estrogen mediated proliferation. There is no classical estrogen response element (ERE) in the cyclin D1 promoter, and induction by ERa has been mapped to an alternative response element, a cyclic-AMP response element (CRE) at –57, with possible participation of an AP-1 site at –954. The action of ERb at the cyclin D1 promoter is unknown, although evidence suggests that ERb may inhibit the proliferative action of ERa. We examined the response of cyclin D1 promoter constructs by luciferase assay and the response of the endogenous protein by western blot in HeLa cells transiently expressing ERa, ERaK206A (a derivative that is superactive at alternative response elements), or ERb. In each case ER activation at the cyclin D1 promoter is mediated by both the CRE and the AP-1 site, which play partly redundant roles. The activation by ERb occurs only with antiestrogens. Estrogens, which activate cyclin D1 gene expression with ERa, inhibit expression with ERb. Strikingly, the presence of ERb completely inhibits cyclin D1 gene activation by estrogen and ERa, or even by estrogen and the superactive ERaK206A. The observation of the opposing action and dominance of ERb over ERa in activation of cyclin D1 gene expression has implications for the postulated role of ERb as a modulator of the proliferative effects of estrogen.


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