ArticleJournal of experimental & clinical cancer research : CR2013
ATM-depletion in breast cancer cells confers sensitivity to PARP inhibition.
Article in Journal of experimental & clinical cancer research : CR, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 94 citations in OpenAlex.
- Integrative multi-omics profiling and machine learning reveal enhancer RNA signatures for early detection and prognostic stratification in breast cancer.NAR cancer · 2026Article
- PARP Inhibitor Sensitivity in Tumors Harboring Non-BRCA Homologous Recombination Gene Alterations: Current Evidence Across Ovarian, Breast, Prostate, and Pancreatic Cancers.International journal of molecular sciences · 2026Review
- Resveratrol potentiates chemotherapeutic efficacy of olaparib in MCF7 human breast cancer cells by inducing apoptosis.Irish journal of medical science · 2026Article
- Interplay Between Poly(ADP-ribosyl)ation and Specific Inner Cellular Events That Suggest Combination Strategies for Overcoming PARP Inhibitor Resistance.Pharmaceutics · 2026Review
- 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
- Tanshinone IIA is synergistic with the PARP inhibitor olaparib in inducing BRCAs-proficient and -deficient triple-negative breast cancer cell apoptosis.Medical oncology (Northwood, London, England) · 2025Article
- PARP-1 as a novel target in endocrine-resistant breast cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- Phase II study of talazoparib in advanced cancers with BRCA1/2, DNA repair, and PTEN alterations.NPJ precision oncology · 2024Article
- PARP inhibitor synthetic lethality in ATM biallelic mutant cancer cell lines is associated with BRCA1/2 and RAD51 downregulation.Frontiers in oncology · 2024Article
- Review
- Review
- Molecular-Targeted Therapy for Tumor-Agnostic Mutations in Acute Myeloid Leukemia.Biomedicines · 2022Review
- RYBP Sensitizes Cancer Cells to PARP Inhibitors by Regulating ATM Activity.International journal of molecular sciences · 2022Article
- Predictive biomarkers for molecularly targeted therapies and immunotherapies in breast cancer.Archives of pharmacal research · 2022Review
- Increased incidence of pathogenic variants in ATM in the context of testing for breast and ovarian cancer predisposition.Journal of human genetics · 2022Article
- Targeting the DNA Damage Response Pathway as a Novel Therapeutic Strategy in Colorectal Cancer.Cancers · 2022Review
- Design and Activity of Novel Oxadiazole Based Compounds That Target Poly(ADP-ribose) Polymerase.Molecules (Basel, Switzerland) · 2022Article
- Homologous Recombination Deficiency in Ovarian, Breast, Colorectal, Pancreatic, Non-Small Cell Lung and Prostate Cancers, and the Mechanisms of Resistance to PARP Inhibitors.Frontiers in oncology · 2022Review
- Expression of MUS81 Mediates the Sensitivity of Castration-Resistant Prostate Cancer to Olaparib.Journal of immunology research · 2022Article
- Role of PARP in TNBC: Mechanism of Inhibition, Clinical Applications, and Resistance.Biomedicines · 2021Review
2 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMutations in the DNA damage response (DDR) factors, breast cancer 1 (BRCA1) and BRCA2, sensitize tumor cells to poly(ADP-ribose) polymerase (PARP) inhibitors. The ataxia telangiectasia mutated (ATM) kinase is a key DDR protein whose heterozygous germline mutation is a moderate-risk factor for developing breast cancer. In this study, we examined whether ATM inactivation in breast cancer cell lines confers sensitivity to PARP inhibitors.
methodsWild-type BRCA1/2 breast cancer cells (i.e., MCF-7 and ZR-75-1 lines) were genetically manipulated to downregulate ATM expression then assayed for cytostaticity/cytotoxicity upon treatment with PARP inhibitors, olaparib and iniparib.
resultsWhen ATM-depleted cells and their relative controls were treated with olaparib (a competitive PARP-1/2 inhibitor) and iniparib (a molecule originally described as a covalent PARP-1 inhibitor) a different response to the two compounds was observed. ATM-depletion sensitized both MCF-7 and ZR-75-1 cells to olaparib-treatment, as assessed by short and long survival assays and cell cycle profiles. In contrast, iniparib induced only a mild, ATM-dependent cytostatic effect in MCF-7 cells whereas ZR-75-1 cells were sensitive to this drug, independently of ATM inactivation. These latest results might be explained by recent observations indicating that iniparib acts with mechanisms other than PARP inhibition.
conclusionsThese data indicate that ATM-depletion can sensitize breast cancer cells to PARP inhibition, suggesting a potential in the treatment of breast cancers low in ATM protein expression/activity, such as those arising in mutant ATM heterozygous carriers.
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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.