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J Biol Chem, Vol. 275, Issue 6, 4532-4536, February 11, 2000

Regulation of BRCA1 Expression by the Rb-E2F Pathway*

Aijin WangDagger §, Robin Schneider-BroussardDagger §, Addanki P. KumarDagger , Michael C. MacLeodDagger , and David G. JohnsonDagger ||

From the Dagger  Department of Carcinogenesis, University of Texas M. D. Anderson Cancer Center, Smithville, Texas 78957

Inheritance of a mutant allele of the breast cancer susceptibility gene BRCA1 confers increased risk of developing breast and ovarian cancers. Likewise, inheritance of a mutant allele of the retinoblastoma susceptibility gene (RB1) results in the development of retinoblastoma and/or osteosarcoma, and both alleles are often mutated or inactivated in sporadic forms of these and other cancers. We now demonstrate that the product of the RB1 gene, Rb, regulates the expression of the murine Brca1 and human BRCA1 genes through its ability to modulate E2F transcriptional activity. The Brca1 gene is identified as an in vivo target of E2F1 in a transgenic mouse model. The Brca1 promoter contains E2F DNA-binding sites that mediate transcriptional activation by E2F1 and repression by Rb. Moreover, ectopic expression of cyclin D1 and Cdk4 can stimulate the Brca1 promoter in an E2F-dependent manner, and this is inhibited by coexpression of the p16INK4a cyclin-dependent kinase inhibitor. The human BRCA1 promoter also contains a conserved E2F site and is similarly regulated by E2F1 and Rb. This functional link between the BRCA1 and Rb tumor suppressors may provide insight into the mechanism by which BRCA1 inactivation contributes to cancer development.

* This work was supported by the Joanne Glass Cancer Research Fund and American Cancer Society Grant RPG-96-001-03-CNE (to M. C. M.), National Institutes of Health Grant CA79648 (to D. G. J.), and NIEHS Center Grants ES07784 and CA16672.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ These authors contributed equally to the work.

Current address: AMC Cancer Research Center, 1600 Pierce St., Lakewood, CO 80214-1897.

|| To whom correspondence should be addressed: Assistant Professor of Carcinogenesis, University of Texas M. D. Anderson Cancer Center, Science Park Research Division, P. O. Box 389, Smithville, TX 78957. Tel.: 512-237-9511; Fax: 512-237-9566; E-mail: djohnson@sprd1. mdacc.tmc.edu.

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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