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Originally published In Press as doi:10.1074/jbc.M201316200 on May 13, 2002

J. Biol. Chem., Vol. 277, Issue 29, 26225-26232, July 19, 2002
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BRCA1 Regulates the Interferon gamma -mediated Apoptotic Response*

Heather N. AndrewsDagger §, Paul B. MullanDagger §, Stewart McWilliamsDagger , Sarka SebelovaDagger , Jennifer E. QuinnDagger , Paula M. GilmoreDagger , Nuala McCabeDagger , Amy Pace, Beverly Koller, Patrick G. JohnstonDagger , Daniel A. Haber||, and D. Paul HarkinDagger **

From the Dagger  Department of Oncology, Cancer Research Centre, The Queen's University Belfast, Belfast BT9 7AB, Northern Ireland, the  Department of Medicine, University of North Carolina, Chapel Hill, North Carolina 27599, and the || Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, Massachusetts 02129

BRCA1 is a tumor suppressor gene implicated in transcriptional regulation. We have generated cell lines with inducible expression of BRCA1 as a tool to identify downstream targets that may be important mediators of BRCA1 function. Oligonucleotide array-based expression profiling identified 11 previously described interferon regulated genes that were up-regulated following inducible expression of BRCA1. Northern blot analysis revealed that a subset of the identified targets including IRF-7, MxA, and ISG-54 were synergistically up-regulated by BRCA1 in the presence of interferon gamma  (IFN-gamma ) but not interferons alpha  or beta . Importantly, IFN-gamma -mediated induction of IRF-7 and MxA was attenuated in the BRCA1 mutant cell line HCC1937, an effect that was rescued following reconstitution of exogenous wild type BRCA1 in these cells. Furthermore, reconstituted BRCA1 sensitized HCC1937 cells to IFN-gamma -induced apoptotic cell death. This study identifies BRCA1 as a component of the IFN-gamma -regulated signaling pathway and suggests that BRCA1 may play a role in the regulation of IFN-gamma -mediated apoptosis.

* This work was supported by Cancer Research Campaign Grant SP2508/0101 and by funds from Action Cancer.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 this work.

** To whom correspondence should be addressed: Dept. of Oncology, Cancer Research Centre, Queen's University of Belfast, University Floor, Belfast City Hospital, Lisburn Rd., Belfast BT9 7AB, N. Ireland. Tel.: 28-9032-9241; Fax: 28-9026-3744; E-mail: d.harkin@qub.ac.uk.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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