ArticleMolecular therapy : the journal of the American Society of Gene Therapy2020
Type 1 Interferon Responses Underlie Tumor-Selective Replication of Oncolytic Measles Virus.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 41 citations in OpenAlex.
- Overcoming Barriers to Clinical Translation: MG1 Maraba Virus as an Emerging Platform for Oncolytic Immunotherapy.Viruses · 2026Review
- A measles virus encoding a CD19/CD3 bispecific T cell engager shows enhanced preclinical anti-BCP-ALL efficacy without significant toxicity.Molecular therapy. Oncology · 2026Article
- Divergent HIV-1 Restriction Phenotypes of IFITMs Expressed in Target Cells and Incorporated into Virions.Biomolecules · 2026Article
- Reovirus resistance in tumors mediated by elevated ISG expression: overcoming therapeutic resistance via JAK/STAT pathway modulation.Virology journal · 2026Article
- Oncolytic Maraba Virus MG1 Mediates Direct and Natural Killer Cell-Dependent Lysis of Ewing Sarcoma.Cancers · 2025Article
- Design and Efficacy of Oncolytic Viruses and Antitumor Vaccines: A Dead End in the Immunotherapy of Pancreatic Cancer?International journal of molecular sciences · 2025Review
- Engineered mesenchymal stem/stromal cells against cancer.Cell death & disease · 2025Review
- Mitochondrial dsRNA from B-ALL cells stimulates mesenchymal stromal cells to become cancer-associated fibroblasts.Blood advances · 2024Article
- A novel approach for breast cancer treatment: the multifaceted antitumor effects of rMeV-Hu191.Hereditas · 2024Article
- Simultaneous Expression of Different Therapeutic Genes by Infection with Multiple Oncolytic HSV-1 Vectors.Biomedicines · 2024Article
- SOCS3 inhibiting JAK-STAT pathway enhances oncolytic adenovirus efficacy by potentiating viral replication and T-cell activation.Cancer gene therapy · 2024Article
- Single-cell RNA sequencing uncovers molecular mechanisms of intravenous immunoglobulin plus methylprednisolone in Kawasaki disease: attenuated monocyte-driven inflammation and improved NK cell cytotoxicity.Frontiers in immunology · 2024Article
- Anti-tumor activity of a recombinant measles virus against canine lung cancer cells.Scientific reports · 2023Article
- Engineering Oncolytic Coxsackievirus A21 with Small Transgenes and Enabling Cell-Mediated Virus Delivery by Integrating Viral cDNA into the Genome.Journal of virology · 2023Article
- Article
- Mesenchymal stromal cells equipped by IFNα empower T cells with potent anti-tumor immunity.Oncogene · 2022Article
- The gamble between oncolytic virus therapy and IFN.Frontiers in immunology · 2022Review
- Peste des Petits Ruminants Virus Exhibits Cell-Dependent Interferon Active Response.Frontiers in cellular and infection microbiology · 2022Article
- Oncolytic Viruses in Combination Therapeutic Approaches with Epigenetic Modulators: Past, Present, and Future Perspectives.Cancers · 2021Review
- Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanism of tumor-selective replication of oncolytic measles virus (MV) is poorly understood. Using a stepwise model of cellular transformation, in which oncogenic hits were additively expressed in human bone marrow-derived mesenchymal stromal cells, we show that MV-induced oncolysis increased progressively with transformation. The type 1 interferon (IFN) response to MV infection was significantly reduced and delayed, in accordance with the level of transformation. Consistently, we observed delayed and reduced signal transducer and activator of transcription (STAT1) phosphorylation in the fully transformed cells. Pre-treatment with IFNβ restored resistance to MV-mediated oncolysis. Gene expression profiling to identify the genetic correlates of susceptibility to MV oncolysis revealed a dampened basal level of immune-related genes in the fully transformed cells compared to their normal counterparts. IFN-induced transmembrane protein 1 (IFITM1) was the foremost basally downregulated immune gene. Stable IFITM1 overexpression in MV-susceptible cells resulted in a 50% increase in cell viability and a significant reduction in viral replication at 24 h after MV infection. Overall, our data indicate that the basal reduction in functions of the type 1 IFN pathway is a major contributor to the oncolytic selectivity of MV. In particular, we have identified IFITM1 as a restriction factor for oncolytic MV, acting at early stages of infection.
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