ArticleVirulence2020
Canine parvovirus induces G1/S cell cycle arrest that involves EGFR Tyr1086 phosphorylation.
Article in Virulence, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 14 citations in OpenAlex.
- A Pharmacologic Approach Against Glioblastoma-A Synergistic Combination of a Quinoxaline-Based and a PI3K/mTOR Dual Inhibitor.International journal of molecular sciences · 2025Article
- Canine parvovirus NS1 induces host translation shutoff by reducing mTOR phosphorylation.Journal of virology · 2025Article
- Parvoviruses NS1 oncolytic attributes: mechanistic insights and synergistic anti-tumor therapeutic strategies.Frontiers in microbiology · 2025Review
- Insights into growth retardation and dwarfism caused by goose parvovirus in goslings: a transcriptomic profiling study.Frontiers in veterinary science · 2025Article
- Overview of Recent Advances in Canine Parvovirus Research: Current Status and Future Perspectives.Microorganisms · 2024Review
- Repurposing Osimertinib and Gedatolisib for Glioblastoma Treatment: Evidence of Synergistic Effects in an In Vitro Phenotypic Study.Pharmaceuticals (Basel, Switzerland) · 2024Article
- For better or worse: crosstalk of parvovirus and host DNA damage response.Frontiers in immunology · 2024Review
- Chaperonin TRiC/CCT subunit CCT7 is involved in the replication of canine parvovirus in F81 cells.Frontiers in microbiology · 2024Article
- Article
- Cold Atmospheric Plasma Boosts Virus Multiplication via EGFR(Tyr1068) Phosphorylation-Mediated Control on Cell Mitophagy.International journal of biological sciences · 2022Article
- Canine Parvovirus and Its Non-Structural Gene 1 as Oncolytic Agents: Mechanism of Action and Induction of Anti-Tumor Immune Response.Frontiers in oncology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Canine parvovirus (CPV) has been used in cancer control as a drug delivery vehicle or anti-tumor reagent due to its multiple natural advantages. However, potential host cell cycle arrest induced by virus infection may impose a big challenge to CPV associated cancer control as it could prevent host cancer cells from undergoing cell lysis and foster them regain viability once the virotherapy was ceased. To explore CPV-induced cell cycle arrest and the underlying mechanism toward improved virotherapeutic design, we focus on epidermal growth factor receptor (EGFR), a cellular receptor interacting with TfR that mediates CPV-host interactions, and alterations on its tyrosine phosphorylation sites in response to CPV infection. We found that CPV could trigger host G1/S cell cycle arrest via the EGFR (Y1086)/p27 and EGFR (Y1068)/STAT3/cyclin D1 axes, and EGFR inhibitor could not reverse this process. Our results contribute to our understandings on the mechanism of CPV-induced host cellular response and can be used in the onco-therapeutic design utilizing CPV by preventing host cancer cells from entering cell cycle arrest.
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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.