Abstract
Abstract Mutations in breast cancer susceptibility genes BRCA1 and BRCA2 predispose individuals to breast and ovarian cancers. Though BRCA associated tumor tissues showed inactivation of both alleles, in primary cells mutations in both copies affect cell viability. This suggests that BRCA1 or 2 loss mediated tumorigenesis process needs other factors. In this study, MSCV (Murine Stem Cell Virus) retroviral mediated insertional mutagenesis approach was used in conditional Brca2 mutant mES (mouse embryonic stem) cells to identify and characterize genetic interactors of BRCA2. One of the factors identified in this screen is brain and reproductive organ expressed protein BRE. BRE is an anti-apoptotic protein and also a component of the BRCA1-A complex that specifically recognizes ‘Lys-63′-linked ubiquitinated histones H2A and H2AX at DNA lesions sites. Overexpression of BRE results into perturbation of DNA damage induced G1/S cell cycle checkpoint by preventing DNA damage induced degradation of CDC25a phosphatase. Further it was found that the stabilization of CDC25a phosphatase in BRE overexpressing cells on DNA damage is mediated via ubiquitin-specific-processing protease 7 (USP7). We are now examining the expression of BRE and CDC25a in BRCA2 deficient tumors. Citation Format: Kajal Biswas, Suhwan Chang, Subha Philip, Shyam K. Sharan. BRE: a genetic interactor of BRCA2. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3952. doi:10.1158/1538-7445.AM2015-3952
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