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[Cancer Research 59, 3547-3551, August 1, 1999]
© 1999 American Association for Cancer Research
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[Cancer Research 59, 3547-3551, August 1, 1999]
© 1999 American Association for Cancer Research

Advances in Brief

BRCA2 Is Required for Ionizing Radiation-induced Assembly of Rad51 Complex in Vivo1

Shyng-Shiou F. Yuan2, Sou-Ying Lee2, Gang Chen2, Meihua Song, Gail E. Tomlinson and Eva Y-H. P. Lee3

Department of Molecular Medicine/Institute of Biotechnology, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78245 [S-S. F. Y., S-Y. L., G. C., M. S., E. Y-H. P. L.], and Department of Pediatrics and the Hamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, Texas 75235 [G. E. T.]

Mutations in BRCA1 and BRCA2 account for the majority of familial breast cancers. Cells with mutated BRCA1 or BRCA2 are hypersensitive to ionizing radiation (IR) and exhibit defective DNA repair. Both BRCA1 and BRCA2 have been reported to bind Rad51, a protein essential for homologous recombination and the recombinational repair of DNA double-strand breaks. In normal cells, a redistribution of Rad51 protein, manifested as formation of Rad51 nuclear foci, is seen upon IR treatment. Here we demonstrate that IR-induced Rad51 foci formation is aberrant in BRCA2- but not BRCA1-deficient tumor cells. In Capan-1 cells, which do not express functional BRCA2, there was little Rad51 foci formation in response to a wide range of radiation dosages. Moreover, forced expression of a fusion protein containing green fluorescent protein and the first Rad51-binding BRC repeat of BRCA2 in cells with wild-type BRCA2 rendered them hypersensitive to IR and cisplatin and compromised IR-induced Rad51 foci formation. In HCC1937 cells, which harbor mutation of BRCA1, IR-induced Rad51 foci were readily detected. This study suggests a requirement of BRCA2 protein for the IR-induced assembly of Rad51 complex in vivo.




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