ArticleThe Journal of clinical investigation2015
Histone deacetylase 6 inhibition enhances oncolytic viral replication in glioma.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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.
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
41 citing papers in PubMed, 68 citations in OpenAlex.
- Accessory microRNA byproducts expand RNA interference via microprocessor-mediated cleavage activation.Science advances · 2026Article
- Oncolytic HSV and cancer drug interactions: Current clinical status and future directions.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Review
- TRIM56 enhances adenoviral E1A steady state to improve oncolytic adenovirus therapy efficacy.Journal of virology · 2025Article
- Epigenetic regulation of histone modifications in glioblastoma: recent advances and therapeutic insights.Biomarker research · 2025Review
- Oncolytic viruses as cancer therapeutics: From mechanistic insights to clinical translation.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Cleavage of HDAC6 to dampen its antiviral activity by nsp5 is a common strategy of swine enteric coronaviruses.Journal of virology · 2024Article
- Transgelin Promotes Glioblastoma Stem Cell Hypoxic Responses and Maintenance Through p53 Acetylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Oncolytic herpes simplex virus armed with a bacterial GBP1 degrader improves antitumor activity.Molecular therapy oncolytics · 2023Article
- Emerging Nano-/Biotechnology Drives Oncolytic Virus-Activated and Combined Cancer Immunotherapy.Research (Washington, D.C.) · 2023Article
- Histone deacetylase 6's function in viral infection, innate immunity, and disease: latest advances.Frontiers in immunology · 2023Review
- Oncolytic herpes simplex viruses for the treatment of glioma and targeting glioblastoma stem-like cells.Frontiers in cellular and infection microbiology · 2023Review
- Histone deacetylase inhibitors enhance oncolytic herpes simplex virus therapy for malignant meningioma.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Article
- Improving cancer immunotherapy by rationally combining oncolytic virus with modulators targeting key signaling pathways.Molecular cancer · 2022Review
- HDAC6 is a prognostic biomarker that mediates IL-13 expression to regulate macrophage polarization through AP-1 in oral squamous cell carcinoma.Scientific reports · 2022Article
- Agent-based computational modeling of glioblastoma predicts that stromal density is central to oncolytic virus efficacy.iScience · 2022Article
- Virally programmed extracellular vesicles sensitize cancer cells to oncolytic virus and small molecule therapy.Nature communications · 2022Article
- Review
- Glioblastoma microenvironment and its reprogramming by oncolytic virotherapy.Frontiers in cellular neuroscience · 2022Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 3 institutions in 1 country.
Funding
Abstract
Oncolytic viral (OV) therapy, which uses genetically engineered tumor-targeting viruses, is being increasingly used in cancer clinical trials due to the direct cytolytic effects of this treatment that appear to provoke a robust immune response against the tumor. As OVs enter tumor cells, intrinsic host defenses have the potential to hinder viral replication and spread within the tumor mass. In this report, we show that histone deacetylase 6 (HDAC6) in tumor cells appears to alter the trafficking of post-entry OVs from the nucleus toward lysosomes. In glioma cell lines and glioma-stem-like cells, HDAC6 inhibition (HDAC6i) by either pharmacologic or genetic means substantially increased replication of oncolytic herpes simplex virus type 1 (oHSV). Moreover, HDAC6i increased shuttling of post-entry oHSV to the nucleus. In addition, electron microscopic analysis revealed that post-entry oHSVs are preferentially taken up into glioma cells through the endosomal pathway rather than via fusion at the cell surface. Together, these findings illustrate a mechanism of glioma cell defense against an incoming infection by oHSV and identify possible approaches to enhance oHSV replication and subsequent lysis of tumor cells.
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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.