53BP1 loss rescues BRCA1 deficiency and is associated with triple-negative and BRCA-mutated breast cancers
Open accessAbstract
Germ-line mutations in breast cancer 1, early onset (BRCA1) result in predisposition to breast and ovarian cancer. BRCA1-mutated tumors show genomic instability, mainly as a consequence of impaired recombinatorial DNA repair. Here we identify p53-binding protein 1 (53BP1) as an essential factor for sustaining the growth arrest induced by Brca1 deletion. Depletion of 53BP1 abrogates the ATM-dependent checkpoint response and G2 cell-cycle arrest triggered by the accumulation of DNA breaks in Brca1-deleted cells. This effect of 53BP1 is specific to BRCA1 function, as 53BP1 depletion did not alleviate proliferation arrest or checkpoint responses in Brca2-deleted cells. Notably, loss of 53BP1 partially restores the homologous-recombination defect of Brca1-deleted cells and reverts their hypersensitivity to DNA-damaging agents. We find reduced 53BP1 expression in subsets of sporadic triple-negative and BRCA-associated breast cancers, indicating the potential clinical implications of our findings.
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BRCA1-deficient cells have homologous recombination defects due to an overactive nonhomologous end-joining pathway.
“In particular, BRCA1-deficient cells have defects in homologous recombination due to an overactive nonhomologous end-joining pathway.”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [76]
Inactivation of 53BP1 restored homologous recombination to BRCA1-deficient cells.
“Remarkably, inactivation of one of these nonhomologous end-joining factors, 53BP1, restored homologous recombination to BRCA1-deficient cells [76,77].”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [76]
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“This activity of BRCA1 is antagonized by 53BP1, which protects broken DNA ends and channels their repair into non-homologous end joining (NHEJ) (Bouwman et al., 2010; Bunting et al., 2010).”
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Self-citation
- Authors
- Bouwman, P., Aly, A., Escandell, J. M., Pieterse, M., Bartkova, J., van der Gulden, H., Hiddingh, S., Thanasoula, M., Kulkarni, A., Yang, Q., Haffty, B. G., Tommiska, J., Blomqvist, C., Drapkin, R., Adams, D. J., Nevanlinna, H., Bartek, J., Tarsounas, M., Ganesan, S., & Jonkers, J.
- Affiliations
- The Netherlands Cancer Institute (NL)
- Rutgers Cancer Institute (US)
- Cancer Research UK (GB)
- Helsinki University Hospital (FI)
- Dana-Farber Cancer Institute (US)
- Wellcome Sanger Institute (GB)
- Corresponding author
- Tarsounas, Madalena
- Ganesan, Shridar
- Jonkers, Jos
- ORCID
- Venue
- Nature Structural & Molecular Biology
- Published
- 2010-05-09
- Volume
- 17
- Issue
- 6
- Pages
- 688-695
- ISSN
- 1545-9985 (ISSN-L)
- 1545-9993
- PMC
- PMC2912507
- OpenAlex
- W2114860131
- Cited by
- 1,001
- References
- 56
- Citations by year
- 2026: 23 · 2025: 43 · 2024: 52 · 2023: 52 · 2022: 70 · 2021: 73 · 2020: 63 · 2019: 60 · 2018: 69 · 2017: 70 · 2016: 65 · 2015: 65 · 2014: 68 · 2013: 95 · 2012: 64
- FWCI
- 29.36
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Structural & Molecular Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Leiden Repository (Leiden University) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
- Funders
- U.S. Department of Defense
- Breast Cancer Research Foundation
- Helsingin ja Uudenmaan Sairaanhoitopiiri
- Wellcome Trust (082356)
- Cancer Research UK (A8784, A6997)
- Breast Cancer Campaign
- National Research Foundation
- Danmarks Grundforskningsfond
- National Cancer Institute
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › BRCA gene mutations in cancer
- Health Sciences › Medicine › Oncology › PARP inhibition in cancer therapy
- Keywords
- 53BP1, BRCA1, BRCA1 deficiency, triple-negative breast cancer, homologous recombination, DNA double-strand break repair, G2 cell cycle arrest, genomic instability, transposon mutagenesis screen, DNA repair
- MeSH terms
- Tumor Suppressor p53-Binding Protein 1, Animals, Breast Neoplasms, Cell Cycle, Chromosomal Proteins, Non-Histone, DNA Damage, DNA Repair, DNA-Binding Proteins, Female, Humans, Mutation, Tumor Cells, Cultured, Mutagenesis, Insertional, Gene Deletion, Mice, Knockout, Drug Resistance, Neoplasm, BRCA1 Protein, Genes, BRCA1, Genes, BRCA2, BRCA2 Protein, Intracellular Signaling Peptides and Proteins, Cell Proliferation, Apoptosis Regulatory Proteins, Mice, Embryonic Stem Cells
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