ArticleOncotarget2016
Loss of CtIP disturbs homologous recombination repair and sensitizes breast cancer cells to PARP inhibitors.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- Germline RBBP8 variants associated with early-onset breast cancer compromise replication fork stability.The Journal of clinical investigation · 2020Trial
- The identity crisis of cryptic lncRNAs: when non-coding RNAs translate into small peptides.The EMBO journal · 2026Review
- Star wars against leukemia: attacking the clones.Leukemia · 2024Review
- A novel RBBP8(p.E281*) germline mutation is a predisposing mutation in familial hereditary cancer syndrome.Journal of molecular medicine (Berlin, Germany) · 2023Article
- Thioparib inhibits homologous recombination repair, activates the type I IFN response, and overcomes olaparib resistance.EMBO molecular medicine · 2023Article
- Clinical application of PARP inhibitors in ovarian cancer: from molecular mechanisms to the current status.Journal of ovarian research · 2023Review
- New perspectives on epigenetic modifications and PARP inhibitor resistance in HR-deficient cancers.Cancer drug resistance (Alhambra, Calif.) · 2023Article
- Epigenetic inactivation of DNA repair genes as promising prognostic and predictive biomarkers in urothelial bladder carcinoma patients.Molecular genetics and genomics : MGG · 2022Article
- Inhibition of WEE1 Potentiates Sensitivity to PARP Inhibitor in Biliary Tract Cancer.Cancer research and treatment · 2022Article
- Sesquiterpene Lactones Potentiate Olaparib-Induced DNA Damage in p53 Wildtype Cancer Cells.International journal of molecular sciences · 2022Article
- New Synthetic Lethality Re-Sensitizing Platinum-Refractory Cancer Cells to Cisplatin In Vitro: The Rationale to Co-Use PARP and ATM Inhibitors.International journal of molecular sciences · 2021Article
- Detection of Molecular Signatures of Homologous Recombination Deficiency in Bladder Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- The lncRNAsMolecular therapy. Nucleic acids · 2021Article
- A stapled peptide mimetic of the CtIP tetramerization motif interferes with double-strand break repair and replication fork protection.Science advances · 2021Article
- Establishment and characterisation of testicular cancer patient-derived xenograft models for preclinical evaluation of novel therapeutic strategies.Scientific reports · 2020Article
- USP52 regulates DNA end resection and chemosensitivity through removing inhibitory ubiquitination from CtIP.Nature communications · 2020Article
- Prognosis value of RBBP8 expression in plasma cell myeloma.Cancer gene therapy · 2020Article
- ATM-dependent activation of SIM2s regulates homologous recombination and epithelial-mesenchymal transition.Oncogene · 2019Article
- AIMP3 Deletion Induces Acute Radiation Syndrome-like Phenotype in Mice.Scientific reports · 2018Article
- Crosstalk of DNA double-strand break repair pathways in poly(ADP-ribose) polymerase inhibitor treatment of breast cancer susceptibility gene 1/2-mutated cancer.Cancer science · 2018Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer is one of the leading causes of death worldwide, and therefore, new and improved approaches for the treatment of breast cancer are desperately needed. CtIP (RBBP8) is a multifunctional protein that is involved in various cellular functions, including transcription, DNA replication, DNA repair and the G1 and G2 cell cycle checkpoints. CtIP plays an important role in homologous recombination repair by interacting with tumor suppressor protein BRCA1. Here, we analyzed the expression profile of CtIP by data mining using published microarray data sets. We found that CtIP expression is frequently decreased in breast cancer patients, and the patient group with low-expressing CtIP mRNA is associated with a significantly lower survival rate. The knockdown of CtIP in breast cancer MCF7 cells reduced Rad51 foci numbers and enhanced f H2AX foci formation after f-irradiation, suggesting that deficiency of CtIP decreases homologous recombination repair and delays DNA double strand break repair. To explore the effect of CtIP on PARP inhibitor therapy for breast cancer, CtIP-depleted MCF7 cells were treated with PARP inhibitor olaparib (AZD2281) or veliparib (ABT-888). As in BRCA mutated cells, PARP inhibitors showed cytotoxicity to CtIP-depleted cells by preventing cells from repairing DNA damage, leading to decreased cell viability. Further, a xenograft tumor model in mice with MCF7 cells demonstrated significantly increased sensitivity towards PARP inhibition under CtIP deficiency. In summary, this study shows that low level of CtIP expression is associated with poor prognosis in breast cancer, and provides a rationale for establishing CtIP expression as a biomarker of PARP inhibitor response, and consequently offers novel therapeutic options for a significant subset of patients.
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Registered trials
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