ArticlePLoS pathogens2020
ATM-mediated DNA double-strand break response facilitated oncolytic Newcastle disease virus replication and promoted syncytium formation in tumor cells.
Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- The multifaceted interactions between Newcastle disease virus proteins and host proteins: a systematic review.Virulence · 2024Pooled it
- Advances in oncolytic virus delivery strategies and challenges in clinical translation.Materials today. Bio · 2026Review
- Oncolytic virus hijacks GOT1 and pyrimidinosomes to fuel pyrimidine synthesis for replication in tumor cells.Tumour virus research · 2026Article
- Integrated transcriptomics, proteomics, and metabolomics analysis reveals newcastle disease virus reshapes glycerophospholipid metabolism.BMC genomics · 2026Article
- Identification of a novel monoclonal antibody derived from the lumpy skin disease virus ORF123 that confers cross-binding and cross-neutralizing activity against Capripoxvirus members.Veterinary research · 2026Article
- Activation of the ATM-Chk2 DNA damage response pathway by Newcastle disease virus enhances viral replication.Veterinary research · 2026Article
- Oncolytic viruses in head and neck cancer: therapeutic promise and translational challenges.Frontiers in immunology · 2026Review
- Case Report: Integration of intratumoral oncolytic adenovirus with total neoadjuvant therapy in metachronous locally advanced rectal cancer.Frontiers in oncology · 2026Article
- Ferroptosis in veterinary medicine: mechanisms, therapies, and unmet challenges.The veterinary quarterly · 2025Review
- L-arginine synergistic with 5-fluorouracil intervenes in DNA damage repair via the DNA-PKcs/ATM/ATR pathway in hepatocellular carcinoma cells.Acta biochimica et biophysica Sinica · 2025Article
- The CRM1-dependent NESVeterinary research · 2025Article
- Seneca Valley virus infection exploits DNA damage response to facilitate viral replication.Journal of virology · 2025Article
- Transcriptomic and Proteomic Analysis of Monkeypox Virus A5L-Expressing HEK293T Cells.International journal of molecular sciences · 2025Article
- Oncolytic Newcastle disease virus induced degradation of YAP through E3 ubiquitin ligase PRKN to exacerbate ferroptosis in tumor cells.Journal of virology · 2024Article
- DNA double-strand break genetic variants in patients with premature ovarian insufficiency.Journal of ovarian research · 2023Review
- Regulation of host factor γ-H2AX level and location by enterovirus A71 for viral replication.Virulence · 2022Article
- SLC1A3 facilitates Newcastle disease virus replication by regulating glutamine catabolism.Virulence · 2022Article
- Porcine Enteric Coronavirus PEDV Induces the ROS-ATM and Caspase7-CAD-γH2AX Signaling Pathways to Foster Its Replication.Viruses · 2022Article
- Single-stranded RNA viruses activate and hijack host apical DNA damage response kinases for efficient viral replication.Genome instability & disease · 2022Article
- Newcastle-disease-virus-induced ferroptosis through nutrient deprivation and ferritinophagy in tumor cells.iScience · 2021Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deoxyribonucleic acid (DNA) damage response (DDR) is the fundamental cellular response for maintaining genomic integrity and suppressing tumorigenesis. The activation of ataxia telangiectasia-mutated (ATM) kinase is central to DNA double-strand break (DSB) for maintaining host-genome integrity in mammalian cells. Oncolytic Newcastle disease virus (NDV) can selectively replicate in tumor cells; however, its influence on the genome integrity of tumor cells is not well-elucidated. Here, we found that membrane fusion and NDV infection triggered DSBs in tumor cells. The late replication and membrane fusion of NDV mechanistically activated the ATM-mediated DSB pathway via the ATM-Chk2 axis, as evidenced by the hallmarks of DSBs, i.e., auto-phosphorylated ATM and phosphorylated H2AX and Chk2. Immunofluorescence data showed that multifaceted ATM-controlled phosphorylation markedly induced the formation of pan-nuclear punctum foci in response to NDV infection and F-HN co-expression. Specific drug-inhibitory experiments on ATM kinase activity further suggested that ATM-mediated DSBs facilitated NDV replication and membrane fusion. We confirmed that the Mre11-RAD50-NBS1 (MRN) complex sensed the DSB signal activation triggered by NDV infection and membrane fusion. The pharmacological inhibition of MRN activity also significantly inhibited intracellular and extracellular NDV replication and syncytia formation. Collectively, these data identified for the first time a direct link between the membrane fusion induced by virus infection and DDR pathways, thereby providing new insights into the efficient replication of oncolytic NDV in tumor cells.
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