ArticleMolecular therapy : the journal of the American Society of Gene Therapy2014
Role of cysteine-rich 61 protein (CCN1) in macrophage-mediated oncolytic herpes simplex virus clearance.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
What it found
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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
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Association BetweenCancer control : journal of the Moffitt Cancer CenterPooled it
- Resistance to oncolytic virotherapy: Multidimensional mechanisms and therapeutic breakthroughs (Review).International journal of molecular medicine · 2025Review
- Oncolytic HSV and cancer drug interactions: Current clinical status and future directions.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- CCN1 Promotes Mesenchymal Phenotype Transition Through Activating NF-κB Signaling Pathway Regulated by S100A8 in Glioma Stem Cells.CNS neuroscience & therapeutics · 2024Article
- Oncolytic virus and tumor-associated macrophage interactions in cancer immunotherapy.Clinical and experimental medicine · 2024Review
- Infection of tumor cells withPNAS nexus · 2024Article
- Downregulation of lncRNA SATB2‑AS1 facilitates glioma cell proliferation by sponging miR‑671‑5p.Experimental and therapeutic medicine · 2023Article
- esRAGE-expressing oHSV enhances anti-tumor efficacy by inhibition of endothelial cell activation.Molecular therapy oncolytics · 2023Article
- Immunosuppressive cells in oncolytic virotherapy for glioma: challenges and solutions.Frontiers in cellular and infection microbiology · 2023Review
- The complex relationship between integrins and oncolytic herpes Simplex Virus 1 in high-grade glioma therapeutics.Molecular therapy oncolytics · 2022Review
- Tumor-Associated Macrophages/Microglia in Glioblastoma Oncolytic Virotherapy: A Double-Edged Sword.International journal of molecular sciences · 2022Review
- Review
- The CREB and AP-1-Dependent Cell Communication Network Factor 1 Regulates Porcine Epidemic Diarrhea Virus-Induced Cell Apoptosis Inhibiting Virus Replication Through the p53 Pathway.Frontiers in microbiology · 2022Article
- Multiple strategies to improve the therapeutic efficacy of oncolytic herpes simplex virus in the treatment of glioblastoma.Oncology letters · 2021Review
- The Current State of Oncolytic Herpes Simplex Virus for Glioblastoma Treatment.Oncolytic virotherapy · 2021Review
- Tumor-Associated Macrophage Status in Cancer Treatment.Cancers · 2020Review
- Anti-viral immunity in the tumor microenvironment: implications for the rational design of herpes simplex virus type 1 oncolytic virotherapy.Current clinical microbiology reports · 2019Article
- Immune therapy, a double-edged sword for oncolytic viruses.Expert opinion on biological therapy · 2019Article
- Review
- Enhancing Therapeutic Efficacy of Oncolytic Herpes Simplex Virus-1 with Integrin β1 Blocking Antibody OS2966.Molecular cancer therapeutics · 2019Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
Glioblastoma is a devastating disease, and there is an urgent need to develop novel therapies, such as oncolytic HSV1 (OV) to effectively target tumor cells. OV therapy depends on tumor-specific replication leading to destruction of neoplastic tissues. Host responses that curtail virus replication limit its efficacy in vivo. We have previously shown that cysteine-rich 61 protein (CCN1) activates a type 1 IFN antiviral defense response in glioblastoma cells. Incorporating TCGA data, we found CCN1 expression to be a negative prognostic factor for glioblastoma patients. Based on this, we used neutralizing antibodies against CCN1 to investigate its effect on OV therapy. Use of an anti-CCN1 antibody in mice bearing glioblastomas treated with OV led to enhanced virus expression along with reduced immune cell infiltration. OV-induced CCN1 increases macrophage migration toward infected glioblastoma cells by directly binding macrophages and also by enhancing the proinflammatory activation of macrophages inducing MCP-1 expression in glioblastoma cells. Activation of macrophages by CCN1 also increases viral clearance. Neutralization of integrin αMβ2 reversed CCN1-induced macrophage activation and migration, and reduced MCP-1 expression by glioblastoma cells. Our findings reveal that CCN1 plays a novel role in pathogen clearance; increasing macrophage infiltration and activation resulting in increased virus clearance in tumors.
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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.