BRE/BRCC45 regulates CDC25A stability by recruiting USP7 in response to DNA damage.
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BRCA2 is essential for maintaining genomic integrity. BRCA2-deficient primary cells are either not viable or exhibit severe proliferation defects. Yet, BRCA2 deficiency contributes to tumorigenesis. It is believed that mutations in genes such as TRP53 allow BRCA2 heterozygous cells to overcome growth arrest when they undergo loss of heterozygosity. Here, we report the use of an insertional mutagenesis screen to identify a role for BRE (Brain and Reproductive organ Expressed, also known as BRCC45), known to be a part of the BRCA1-DNA damage sensing complex, in the survival of BRCA2-deficient mouse ES cells. Cell viability by BRE overexpression is mediated by deregulation of CDC25A phosphatase, a key cell cycle regulator and an oncogene. We show that BRE facilitates deubiquitylation of CDC25A by recruiting ubiquitin-specific-processing protease 7 (USP7) in the presence of DNA damage. Additionally, we uncovered the role of CDC25A in BRCA-mediated tumorigenesis, which can have implications in cancer treatment.
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USP7 negatively regulates Chk1-mediated cell cycle arrest by deubiquitinating and stabilizing Cdc25A in response to DNA damage, recruited via BRE.
“Interestingly, USP7 also negatively regulates Chk1-mediated cell cycle arrest, by deubiquitinating and stabilizing Cdc25A in response to DNA damage. Here, USP7 is recruited via an interaction with the Cdc25A-interactor, BRE (Biswas et al., 2018).”
From USP7 Is a Master Regulator of Genome Stability (2020) · cites this paper as Biswas et al., 2018
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- Authors
- Biswas, K., Philip, S., Yadav, A., Martin, B. K., Burkett, S., Singh, V., Babbar, A., North, S. L., Chang, S., & Sharan, S. K.
- Affiliations
- National Cancer Institute (US)
- Frederick National Laboratory for Cancer Research (US)
- University of Ulsan (KR)
- Corresponding author
- Sharan, Shyam K.
- Venue
- Nature Communications
- Published
- 2018-02-07
- Volume
- 9
- Issue
- 1
- Pages
- 537-537
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC5803202
- OpenAlex
- W2806476124
- Cited by
- 41
- References
- 74
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2023: 8 · 2022: 2 · 2021: 3 · 2020: 12 · 2019: 9 · 2018: 2
- FWCI
- 2.31
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- York University
- National Institutes of Health
- National Cancer Institute
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › BRCA gene mutations in cancer
- Keywords
- BRCA2, BRe, CDC25A, USP7, deubiquitination, DNA damage response, carcinogenesis, oncogene deregulation, genome stability
- MeSH terms
- Ubiquitin-Specific Peptidase 7, Animals, Cell Survival, Cells, Cultured, DNA Damage, Enzyme Stability, Heterozygote, Humans, Nerve Tissue Proteins, Protein Processing, Post-Translational, Tumor Suppressor Protein p53, Mutagenesis, Insertional, Mice, Knockout, BRCA1 Protein, Loss of Heterozygosity, cdc25 Phosphatases, BRCA2 Protein, Mice, Ubiquitination, MCF-7 Cells, Carcinogenesis
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