ArticleJournal of virology2013
Innate immune defense defines susceptibility of sarcoma cells to measles vaccine virus-based oncolysis.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 57 citations in OpenAlex.
- Article
- Biomarker screen for efficacy of oncolytic virotherapy in patient-derived pancreatic cancer cultures.EBioMedicine · 2024Article
- Personalizing Oncolytic Immunovirotherapy Approaches.Molecular diagnosis & therapy · 2024Article
- In Vitro Sensitivity of Neuroendocrine Neoplasms to an Armed Oncolytic Measles Vaccine Virus.Cancers · 2024Article
- Immune responses elicited by ssRNA(-) oncolytic viruses in the host and in the tumor microenvironment.Journal of cancer metastasis and treatment · 2023Article
- NK Cell Effector Functions and Bystander Tumor Cell Killing in Immunovirotherapy.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Virotherapy in Germany-Recent Activities in Virus Engineering, Preclinical Development, and Clinical Studies.Viruses · 2021Review
- Personalizing Oncolytic Virotherapy for Glioblastoma: In Search of Biomarkers for Response.Cancers · 2021Review
- Measles Virus as an Oncolytic Immunotherapy.Cancers · 2021Review
- Assessing and Overcoming Resistance Phenomena against a Genetically Modified Vaccinia Virus in Selected Cancer Cell Lines.International journal of molecular sciences · 2020Article
- Type 1 Interferon Responses Underlie Tumor-Selective Replication of Oncolytic Measles Virus.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- Biological treatment of pediatric sarcomas by combined virotherapy and NK cell therapy.BMC cancer · 2019Article
- Chemovirotherapy for pancreatic cancer: Gemcitabine plus oncolytic measles vaccine virus.Oncology letters · 2019Article
- The lytic activity of VSV-GP treatment dominates the therapeutic effects in a syngeneic model of lung cancer.British journal of cancer · 2019Article
- Suicide gene‑armed measles vaccine virus for the treatment of AML.International journal of oncology · 2019Article
- Article
- Synergistic Effects of Bortezomib-OV Therapy and Anti-Invasive Strategies in Glioblastoma: A Mathematical Model.Cancers · 2019Article
- Defects in interferon pathways as potential biomarkers of sensitivity to oncolytic viruses.Reviews in medical virology · 2018Review
- Engineered Oncolytic Poliovirus PVSRIPO Subverts MDA5-Dependent Innate Immune Responses in Cancer Cells.Journal of virology · 2018Article
- Measles Vaccine.Viral immunology · 2018Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The oncolytic potential of measles vaccine virus (MeV) has been demonstrated in several tumor entities. Here, we investigated the susceptibility of eight sarcoma cell lines to MeV-mediated oncolysis and found five to be susceptible, whereas three proved to be resistant. In the MeV-resistant cell lines, we often observed an inhibition of viral replication along with a strong upregulation of the intracellular virus-sensing molecule RIG-I and of the interferon (IFN)-stimulated gene IFIT1. Not only expression of IFIT1 but also phosphorylation of IFN-stimulated Stat1 took place rapidly and were found to be persistent over time. In contrast, susceptible cell lines showed a much weaker, delayed, or completely missing expression of IFIT1 as well as a delayed or only transient phosphorylation of Stat1, whereas exogenic stimulation with beta interferon (IFN-β) resulted in a comparable profound activation of Stat1 and expression of IFIT1 in all cell lines. Pretreatment with IFN-β rendered three of the susceptible cell lines more resistant to MeV-mediated oncolysis. These data suggest that differences in the innate immune defense often account for different degrees of susceptibility of sarcoma cell lines to MeV-mediated oncolysis. From a therapeutic perspective, we were able to overcome resistance to MeV by increasing the multiplicity of infection (MOI) and by addition of the prodrug 5-fluorocytosine (FC), thereby exploiting the suicide gene function of virotherapeutic vector MeV-SCD armed with the SCD fusion protein, which consists of yeast cytosine deaminase and yeast uracil phosphoribosyltransferase.
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