ArticleBMC cancer2016
53BP1 depletion causes PARP inhibitor resistance in ATM-deficient breast cancer cells.
Article in BMC cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Interplay Between Poly(ADP-ribosyl)ation and Specific Inner Cellular Events That Suggest Combination Strategies for Overcoming PARP Inhibitor Resistance.Pharmaceutics · 2026Review
- SIRT2 mitigates radiation-induced oral mucositis by promoting homologous recombination-mediated DNA double-strand break repair in epithelial stem cells.Cancer letters · 2026Article
- GSK3B directs DNA repair choice and determines tumor response to PARP1 inhibition independent of BRCA1.The Journal of clinical investigation · 2025Article
- Poly(ADP-ribose) polymerase-1 in breast cancers: expression level and its association in various molecular subtypes with a focus in Africa.Discover oncology · 2025Review
- SETD1A-dependent EME1 transcription drives PARPi sensitivity in HR deficient tumour cells.British journal of cancer · 2025Article
- Ferrocene thiazolidine-2,4-dione derivatives cause DNA damage and interfere with DNA repair in triple-negative breast cancer cells.PloS one · 2025Article
- Inhibition of CXorf56 promotes PARP inhibitor-induced cytotoxicity in triple-negative breast cancer.NPJ breast cancer · 2023Article
- Inhibition of BAD-Ser99 phosphorylation synergizes with PARP inhibition to ablate PTEN-deficient endometrial carcinoma.Cell death & disease · 2022Article
- PARP inhibitor resistance in breast and gynecological cancer: Resistance mechanisms and combination therapy strategies.Frontiers in pharmacology · 2022Review
- Therapeutic vulnerability to PARP1,2 inhibition in RB1-mutant osteosarcoma.Nature communications · 2021Article
- Inhibition of DNA Repair in Cancer Therapy: Toward a Multi-Target Approach.International journal of molecular sciences · 2020Review
- Recent advancements in PARP inhibitors-based targeted cancer therapy.Precision clinical medicine · 2020Review
- Resistance Mechanisms to Taxanes and PARP Inhibitors in Advanced Prostate Cancer.Current opinion in endocrine and metabolic research · 2020Article
- Article
- State-of-the-art strategies for targeting the DNA damage response in cancer.Nature reviews. Clinical oncology · 2019Review
- Synthetically Lethal BMN 673 (Talazoparib) Loaded Solid Lipid Nanoparticles for BRCA1 Mutant Triple Negative Breast Cancer.Pharmaceutical research · 2018Article
- Acquired resistance of phosphatase and tensin homolog-deficient cells to poly(ADP-ribose) polymerase inhibitor and Ara-C mediated by 53BP1 loss and SAMHD1 overexpression.Cancer science · 2018Article
- PARP1 expression and its correlation with survival is tumour molecular subtype dependent in glioblastoma.Oncotarget · 2017Article
- Combining 53BP1 with BRCA1 as a biomarker to predict the sensitivity of poly(ADP-ribose) polymerase (PARP) inhibitors.Acta pharmacologica Sinica · 2017Article
- Erratum to: 53BP1 depletion causes PARP inhibitor resistance in ATM-deficient breast cancer cells.BMC cancer · 2016Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMutations in DNA damage response factors BRCA1 and BRCA2 confer sensitivity to poly(ADP-ribose) polymerase (PARP) inhibitors in breast and ovarian cancers. BRCA1/BRCA2-defective tumors can exhibit resistance to PARP inhibitors via multiple mechanisms, one of which involves loss of 53BP1. Deficiency in the DNA damage response factor ataxia-telangiectasia mutated (ATM) can also sensitize tumors to PARP inhibitors, raising the question of whether the presence or absence of 53BP1 can predict sensitivity of ATM-deficient breast cancer to these inhibitors.
methodsCytotoxicity of PARP inhibitor and ATM inhibitor in breast cancer cell lines was assessed by MTS, colony formation and apoptosis assays. ShRNA lentiviral vectors were used to knockdown 53BP1 expression in breast cancer cell lines. Phospho-ATM and 53BP1 protein expressions were determined in human breast cancer tissues by immunohistochemistry (IHC).
resultsWe show that inhibiting ATM increased cytotoxicity of PARP inhibitor in triple-negative and non-triple-negative breast cancer cell lines, and depleting the cells of 53BP1 reduced this cytotoxicity. Inhibiting ATM abrogated homologous recombination induced by PARP inhibitor, and down-regulating 53BP1 partially reversed this effect. Further, overall survival was significantly better in triple-negative breast cancer patients with lower levels of phospho-ATM and tended to be better in patients with negative 53BP1.
conclusionThese results suggest that 53BP1 may be a predictor of PARP inhibitor resistance in patients with ATM-deficient tumors.
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