ArticleOncogene2010
Rac1 is required for oncolytic NDV replication in human cancer cells and establishes a link between tumorigenesis and sensitivity to oncolytic virus.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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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.
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Who cites it
38 citing papers in PubMed, 62 citations in OpenAlex.
- In situ APMV-4 vaccination primes systemic response to subtherapeutic dosing of aCTLA-4 in colorectal carcinoma.Journal for immunotherapy of cancer · 2026Article
- Genetic Regulation of ERK1/2-c-Fos Signalling Pathway in Newcastle Disease Virus-Induced Apoptosis of Human Pancreatic Cancer Stem Cells.The Malaysian journal of medical sciences : MJMS · 2026Article
- A noncarcinoma mouse cell line is nonsusceptible to Newcastle disease virus established by spontaneous immortalization.Scientific reports · 2025Article
- Review
- Molecular Circuits of Immune Sensing and Response to Oncolytic Virotherapy.International journal of molecular sciences · 2024Review
- Article
- Counteracting Immunosuppression in the Tumor Microenvironment by Oncolytic Newcastle Disease Virus and Cellular Immunotherapy.International journal of molecular sciences · 2022Review
- Avian Paramyxovirus 4 Antitumor Activity Leads to Complete Remissions and Long-term Protective Memory in Preclinical Melanoma and Colon Carcinoma Models.Cancer research communications · 2022Article
- Molecular Mechanisms of Anti-Neoplastic and Immune Stimulatory Properties of Oncolytic Newcastle Disease Virus.Biomedicines · 2022Review
- The phosphatase and tensin homolog gene inserted between NP and P gene of recombinant New castle disease virus oncolytic effect test to glioblastoma cell and xenograft mouse model.Virology journal · 2022Article
- An Extensive Review on Preclinical and Clinical Trials of Oncolytic Viruses Therapy for Pancreatic Cancer.Frontiers in oncology · 2022Review
- MSCs loaded with oncolytic reovirus: migration and in vivo virus delivery potential for evaluating anti-cancer effect in tumor-bearing C57BL/6 mice.Cancer cell international · 2021Article
- Less Can Be More: The Hormesis Theory of Stress Adaptation in the Global Biosphere and Its Implications.Biomedicines · 2021Review
- Oncolytic Virotherapy: The Cancer Cell Side.Cancers · 2021Review
- Personalizing Oncolytic Virotherapy for Glioblastoma: In Search of Biomarkers for Response.Cancers · 2021Review
- Advances in the Study of Antitumour Immunotherapy for Newcastle Disease Virus.International journal of medical sciences · 2021Review
- Oncolytic Virotherapy in Glioma Tumors.International journal of molecular sciences · 2020Review
- 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
- Antiviral interferons induced by Newcastle disease virus (NDV) drive a tumor-selective apoptosis.Scientific reports · 2019Article
- Breaking Therapy Resistance: An Update on Oncolytic Newcastle Disease Virus for Improvements of Cancer Therapy.Biomedicines · 2019Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oncolytic Newcastle disease virus (NDV) replicates selectively in most human tumor cells but not in normal cells. The relationship between tumorigenesis and the selective susceptibility of most tumor cells to oncolytic NDV replication is poorly understood. A multistage skin carcinogenesis model derived from non-tumorigenic HaCaT cells was used to systematically investigate the molecular mechanisms involved in the oncolytic NDV-sensitivity associated with tumorigenic transformation. No significant differences in interferon signaling were observed between the virus-sensitive tumor cells and the virus-resistant non-tumorigenic parental cells. Oncogenic H-Ras, which had been used for tumorigenic transformation, was shown to be necessary for virus replication but was not sufficient to render cells susceptible to NDV replication. By using an siRNA screening approach to search for virus-sensitizing genes in the tumorigenic cells, we could identify the small GTPase Rac1 as an oncogenic protein that is essential for NDV replication and anchorage-independent growth in tumorigenic cells. Furthermore, Rac1 expression was sufficient to render non-tumorigenic cells susceptible to NDV replication and to oncolytic cytotoxicity. This study establishes Rac1 as a link between tumorigenesis and oncolytic virus sensitivity in the HaCaT multistage skin carcinogenesis model.
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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.