ArticleNAR cancer2020
Intrinsic ATR signaling shapes DNA end resection and suppresses toxic DNA-PKcs signaling.
Article in NAR cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed.
- Mechanisms and regulation of DNA end resection in the maintenance of genome stability.Nature reviews. Molecular cell biology · 2025Review
- Reversing regulatory safeguards: Targeting the ATR pathway to overcome PARP inhibitor resistance.Molecular therapy. Oncology · 2025Review
- Targeting replication stress in cancer therapy.Nature reviews. Drug discovery · 2023Review
- ATR Inhibitors in Platinum-Resistant Ovarian Cancer.Cancers · 2022Review
- DNA-PKcs promotes fork reversal and chemoresistance.Molecular cell · 2022Article
- Cell cycle checkpoints and beyond: Exploiting the ATR/CHK1/WEE1 pathway for the treatment of PARP inhibitor-resistant cancer.Pharmacological research · 2022Review
- Selective vulnerability of ARID1A deficient colon cancer cells to combined radiation and ATR-inhibitor therapy.Frontiers in oncology · 2022Article
- EXO5-DNA structure and BLM interactions direct DNA resection critical for ATR-dependent replication restart.Molecular cell · 2021Article
- To Join or Not to Join: Decision Points Along the Pathway to Double-Strand Break Repair vs. Chromosome End Protection.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Most cancer cells experience oncogene-induced replication stress and, as a result, exhibit high intrinsic activation of the ATR kinase. Although cancer cells often become more dependent on ATR for survival, the precise mechanism by which ATR signaling ensures cancer cell fitness and viability remains incompletely understood. Here, we find that intrinsic ATR signaling is crucial for the ability of cancer cells to promote DNA end resection, the first step in homology-directed DNA repair. Inhibition of ATR over multiple cell division cycles depletes the pool of pro-resection factors and prevents the engagement of RAD51 as well as RAD52 at nuclear foci, leading to toxic DNA-PKcs signaling and hypersensitivity to PARP inhibitors. The effect is markedly distinct from acute ATR inhibition, which blocks RAD51-mediated repair but not resection and engagement of RAD52. Our findings reveal a key pro-resection function for ATR and define how ATR inhibitors can be used for effective manipulation of DNA end resection capacity and DNA repair outcomes in cancer cells.
Identifiers
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Registered trials
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.