RAD51 up-regulation bypasses BRCA1 function and is a common feature of BRCA1-deficient breast tumors.

RAD51 up-regulation bypasses BRCA1 function and is a common feature of BRCA1-deficient breast tumors. Research Abstract Details 

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RAD51 up-regulation bypasses BRCA1 function and is a common feature of BRCA1-deficient breast tumors. Abstract Text:

Richard W Martin,Brian J Orelli,Mitsuyoshi Yamazoe,Andy J Minn,Shunichi Takeda,Douglas K Bishop,Richard W Martin,Brian J Orelli,Mitsuyoshi Yamazoe,Andy J Minn,Shunichi Takeda,Douglas K Bishop,

The breast cancer susceptibility gene BRCA1 encodes a large protein thought to contribute to a variety of cellular processes, although the critical determinants of BRCA1-deficient tumorigenesis remain unclear. Given that BRCA1 is required for cell proliferation, suppressor mutations are believed to modify BRCA1 phenotypes and contribute to the etiology of BRCA1-deficient tumors. Here, we show that overexpression of the homologous recombinase RAD51 in a DT40 BRCA1Delta/Delta mutant rescues defects in proliferation, DNA damage survival, and homologous recombination (HR). In addition, epistasis analysis with BRCA1 and the DNA end-joining factor KU70 indicates that these factors operate independently of one another to repair double-strand breaks. Consistent with this genetic finding, cell synchronization studies show that the ability of BRCA1 to promote radioresistance is restricted to the late S and G2 phases of the cell cycle, as predicted for genes whose function is specific to homology-mediated repair rather than nonhomologous end-joining. Notably, retrospective analyses of microarray expression data reveal elevated expression of RAD51 and two of its late-acting cofactors, RAD54 and RAD51AP1, in BRCA1-deficient versus sporadic breast tumors. Taken together, our results indicate that up-regulation of HR provides a permissive genetic context for cells lacking BRCA1 function by circumventing its requirement in RAD51 subnuclear assembly. Furthermore, the data support a model in which enhanced HR activity contributes to the etiology of BRCA1-deficient tumors.

RAD51 up-regulation bypasses BRCA1 function and is a common feature of BRCA1-deficient breast tumors. Publishing Authors By Initials

RW Martin,BJ Orelli,M Yamazoe,AJ Minn,S Takeda,DK Bishop,RW Martin,BJ Orelli,M Yamazoe,AJ Minn,S Takeda,DK Bishop,

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RAD51 up-regulation bypasses BRCA1 function and is a common feature of BRCA1-deficient breast tumors. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Cancer research

VOLUME: 67

Page Numbers: 9658-65

Journal Abbreviation: Cancer Res.

ISSN: 0008-5472

DAY: 15

MONTH: Oct

YEAR: 2007

RAD51 up-regulation bypasses BRCA1 function and is a common feature of BRCA1-deficient breast tumors. Information

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LANGUAGE: eng

NlmUniqueID: 2984705

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Grant and Affiliation Information for RAD51 up-regulation bypasses BRCA1 function and is a common feature of BRCA1-deficient breast tumors.

AFFILIATION: Department of Radiation, Ludwig Center for Metastasis Research, University of Chicago, Chicago, Illinois 60637, USA.

Country: United States

AGENCY: United States NCI

GRANT: R01 CA095777

ACRONYM: CA

MEDLINETA: Cancer Res

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