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Ref Type Journal Article
PMID (25368520)
Authors Lee PS, Fang J, Jessop L, Myers T, Raj P, Hu N, Wang C, Taylor PR, Wang J, Khan J, Jasin M, Chanock SJ
Title RAD51B Activity and Cell Cycle Regulation in Response to DNA Damage in Breast Cancer Cell Lines.
Journal Vol Issue Date Pages Journal Short Title
Breast cancer : basic and clinical research 8 2014 135-44 Breast Cancer (Auckl)
URL
Abstract Text Common genetic variants mapping to two distinct regions of RAD51B, a paralog of RAD51, have been associated with breast cancer risk in genome-wide association studies (GWAS). RAD51B is a plausible candidate gene because of its established role in the homologous recombination (HR) process. How germline genetic variation in RAD51B confers susceptibility to breast cancer is not well understood. Here, we investigate the molecular function of RAD51B in breast cancer cell lines by knocking down RAD51B expression by small interfering RNA and treating cells with DNA-damaging agents, namely cisplatin, hydroxyurea, or methyl-methanesulfonate. Our results show that RAD51B-depleted breast cancer cells have increased sensitivity to DNA damage, reduced efficiency of HR, and altered cell cycle checkpoint responses. The influence of RAD51B on the cell cycle checkpoint is independent of its role in HR and further studies are required to determine whether these functions can explain the RAD51B breast cancer susceptibility alleles.

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Molecular Profile Treatment Approach
Gene Name Source Synonyms Protein Domains Gene Description Gene Role
Therapy Name Drugs Efficacy Evidence Clinical Trials
Drug Name Trade Name Synonyms Drug Classes Drug Description
Gene Variant Impact Protein Effect Variant Description Associated with drug Resistance
Molecular Profile Indication/Tumor Type Response Type Therapy Name Approval Status Evidence Type Efficacy Evidence References
RAD51B wild-type breast cancer not applicable N/A Preclinical Emerging SiRNA inhibition of RAD51B in breast cancer cells resulted in increased sensitivity to DNA damaging agents in culture, suggesting that RAD51B could be a promising therapeutic target for sensitization to chemotherapeutic agents in combination therapies (PMID: 25368520). 25368520