ArticleJournal of virology2007
p53-independent endoplasmic reticulum stress-mediated cytotoxicity of a Newcastle disease virus strain in tumor cell lines.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
40 citing papers in PubMed, 88 citations in OpenAlex.
- Antiviral Effects of Avian Interferon-Stimulated Genes.Animals : an open access journal from MDPI · 2024Review
- Newcastle Disease Virus Virotherapy: Unveiling Oncolytic Efficacy and Immunomodulation.Biomedicines · 2024Article
- The Viral Knock: Ameliorating Cancer Treatment with Oncolytic Newcastle Disease Virus.Life (Basel, Switzerland) · 2023Review
- Oncolytic virotherapy: basic principles, recent advances and future directions.Signal transduction and targeted therapy · 2023Review
- Article
- Review
- Evaluation of Apoptosis Induction by Newcastle Disease Virus LaSota Strain in Human Breast Carcinoma Cells.Archives of Razi Institute · 2020Article
- Newcastle Disease virus infection activates PI3K/Akt/mTOR and p38 MAPK/Mnk1 pathways to benefit viral mRNA translation via interaction of the viral NP protein and host eIF4E.PLoS pathogens · 2020Article
- Review
- Antiviral interferons induced by Newcastle disease virus (NDV) drive a tumor-selective apoptosis.Scientific reports · 2019Article
- Newcastle disease virus mediated apoptosis and migration inhibition of human oral cancer cells: A probable role of β-catenin and matrix metalloproteinase-7.Scientific reports · 2019Article
- Article
- Newcastle Disease Virus Establishes Persistent Infection in Tumor CellsJournal of virology · 2017Article
- RIP1 is a central signaling protein in regulation of TNF-α/TRAIL mediated apoptosis and necroptosis during Newcastle disease virus infection.Oncotarget · 2017Article
- Oncolytic Viruses-Interaction of Virus and Tumor Cells in the Battle to Eliminate Cancer.Frontiers in oncology · 2017Review
- Recombinant Newcastle disease virus expressing P53 demonstrates promising antitumor efficiency in hepatoma model.Journal of biomedical science · 2016Article
- Fifty Years of Clinical Application of Newcastle Disease Virus: Time to Celebrate!Biomedicines · 2016Review
- Newcastle disease virus, rituximab, and doxorubicin combination as anti-hematological malignancy therapy.Oncolytic virotherapy · 2016Article
- The therapeutic effect of death: Newcastle disease virus and its antitumor potential.Virus research · 2015Review
- Antineoplastic activity of Newcastle disease virus strain D90 in oral squamous cell carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While Newcastle disease virus (NDV) causes serious infections in birds, it is apparently nonpathogenic in mammalian species, including humans. Previous observations and small-scale clinical trials indicated that NDV exerts oncolytic effects. Isolates of NDV were found to have selective affinity to transformed cells. We previously showed that the attenuated NDV strain MTH-68/H causes apoptotic cell death in cultures of PC12 rat pheochromocytoma cells. The aim of the present study was to extend MTH-68/H cytotoxicity testing with human tumor cell lines and to analyze certain biochemical aspects of its oncolytic effect. MTH-68/H was found to be able to kill a wide range of transformed cells by apoptosis. While caspase-8 and caspase-9 are not involved in MTH-68/H-induced apoptosis, activation of caspase-3 and caspase-12 was detected in virus-infected PC12 cells. A human glioblastoma cell line with repressible expression of the p53 protein did not show any difference in MTH-68/H sensitivity in its p53-expressing and p53-depleted states, indicating that the apoptotic process induced by MTH-68/H does not depend on p53. Apoptosis was accompanied by virus replication in two tumor cell lines tested (PC12 cells and HeLa human cervical cells), and signs of endoplasmic reticulum stress (phosphorylation of protein kinase R-like endoplasmic reticulum kinase and eIF2alpha) were also detected in transformed cells. In contrast, proliferation of nontransformed mouse and rat fibroblast cell lines and human primary fibroblasts was not affected by MTH-68/H treatment. MTH-68/H thus selectively kills tumor cell cultures by inducing endoplasmic reticulum stress leading to p53-independent apoptotic cell death.
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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.