ArticleBreast cancer : basic and clinical research2014
RAD51B Activity and Cell Cycle Regulation in Response to DNA Damage in Breast Cancer Cell Lines.
Article in Breast cancer : basic and clinical research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Meta-analysis of the association between overexpression of RAD51 family genes and prognosis and clinical features in breast cancer.Scientific reports · 2025Pooled it
- Establishing Patient-Derived Cancer Cell Cultures and Xenografts in Biliary Tract Cancer.Cancer research and treatment · 2023Article
- Loss of TRP53 (p53) accelerates tumorigenesis and changes the tumor spectrum of SJL/J mice.Genes & cancer · 2020Article
- Pine needle oil induces G2/M arrest of HepG2 cells by activating the ATM pathway.Experimental and therapeutic medicine · 2018Article
- Overexpression of RAD51B predicts a preferable prognosis for non-small cell lung cancer patients.Oncotarget · 2017Article
- Predicting Triple-Negative Breast Cancer Subtype Using Multiple Single Nucleotide Polymorphisms for Breast Cancer Risk and Several Variable Selection Methods.Geburtshilfe und Frauenheilkunde · 2017Article
- Whole-Genome Sequencing Reveals Diverse Models of Structural Variations in Esophageal Squamous Cell Carcinoma.American journal of human genetics · 2016Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.