ArticleJournal of virology2014
Histone deacetylase inhibitors potentiate vesicular stomatitis virus oncolysis in prostate cancer cells by modulating NF-κB-dependent autophagy.
Article in Journal of virology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 84 citations in OpenAlex.
- Autophagy induction by histone deacetylase inhibitors inhibits HIV type 1.The Journal of biological chemistry · 2015Trial
- Reovirus resistance in tumors mediated by elevated ISG expression: overcoming therapeutic resistance via JAK/STAT pathway modulation.Virology journal · 2026Article
- Oncolytic viruses: advanced strategies in cancer therapy.Signal transduction and targeted therapy · 2026Review
- Defining the heterogeneous molecular landscape of lung cancer cell responses to epigenetic inhibition.Communications biology · 2026Article
- Employing the Oncolytic Vesicular Stomatitis Virus in Cancer Virotherapy: Resistance and Clinical Considerations.Viruses · 2024Review
- Role of Autophagy in Type 2 Diabetes Mellitus: The Metabolic Clash.Journal of cellular and molecular medicine · 2024Review
- Review
- Matrix Protein of Vesicular Stomatitis Virus Targets the Mitochondria, Reprograms Glucose Metabolism, and Sensitizes to 2-Deoxyglucose in Glioblastoma.Human gene therapy · 2024Article
- Oncolytic vesicular stomatitis virus alone or in combination with JAK inhibitors is effective against ovarian cancer.Molecular therapy. Oncology · 2024Article
- Octyl itaconate enhances VSVΔ51 oncolytic virotherapy by multitarget inhibition of antiviral and inflammatory pathways.Nature communications · 2024Article
- Histone deacetylase inhibitors: targeting epigenetic regulation in the treatment of acute leukemia.Therapeutic advances in hematology · 2024Review
- The role of viruses in cancer development versus cancer therapy: An oncological perspective.Cancer medicine · 2023Review
- Autophagy: A Potential Therapeutic Target to Tackle Drug Resistance in Multiple Myeloma.International journal of molecular sciences · 2023Review
- Cellular resistance to an oncolytic virus is driven by chronic activation of innate immunity.iScience · 2023Article
- A Genome-Wide CRISPR-Cas9 Loss-of-Function Screening to Identify Host Restriction Factors Modulating Oncolytic Virotherapy.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Emetine in Combination with Chloroquine Induces Oncolytic Potential of HIV-1-Based Lentiviral Particles.Cells · 2022Article
- SARS-CoV-2 3CLpro whole human proteome cleavage prediction and enrichment/depletion analysis.Computational biology and chemistry · 2022Article
- Virally programmed extracellular vesicles sensitize cancer cells to oncolytic virus and small molecule therapy.Nature communications · 2022Article
- HDAC inhibitors: Targets for tumor therapy, immune modulation and lung diseases.Translational oncology · 2022Review
- Potentiating effect of reovirus on immune checkpoint inhibition in microsatellite stable colorectal cancer.Frontiers in oncology · 2022Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Vesicular stomatitis virus (VSV) is an oncolytic virus that induces cancer cell death through activation of the apoptotic pathway. Intrinsic resistance to oncolysis is found in some cell lines and many primary tumors as a consequence of residual innate immunity to VSV. In resistant-tumor models, VSV oncolytic potential can be reversibly stimulated by combination with epigenetic modulators, such as the histone deacetylase inhibitor vorinostat. Based on this reversible effect of vorinostat, we reasoned that critical host genes involved in oncolysis may likewise be reversibly regulated by vorinostat. A transcriptome analysis in prostate cancer PC3 cells identified a subset of NF-κB target genes reversibly regulated by vorinostat, as well as a group of interferon (IFN)-stimulated genes (ISGs). Consistent with the induction of NF-κB target genes, vorinostat-mediated enhancement of VSV oncolysis increased hyperacetylation of NF-κB RELA/p65. Additional bioinformatics analysis revealed that NF-κB signaling also increased the expression of several autophagy-related genes. Kinetically, autophagy preceded apoptosis, and apoptosis was observed only when cells were treated with both VSV and vorinostat. VSV replication and cell killing were suppressed when NF-κB signaling was inhibited using pharmacological or genetic approaches. Inhibition of autophagy by 3-methyladenine (3-MA) enhanced expression of ISGs, and either 3-MA treatment or genetic ablation of the autophagic marker Atg5 decreased VSV replication and oncolysis. Together, these data demonstrate that vorinostat stimulates NF-κB activity in a reversible manner via modulation of RELA/p65 signaling, leading to induction of autophagy, suppression of the IFN-mediated response, and subsequent enhancement of VSV replication and apoptosis.
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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.