ArticleCancer research2012
Extracellular matrix protein CCN1 limits oncolytic efficacy in glioma.
Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
43 citing papers in PubMed, 56 citations in OpenAlex.
- CCN1 as a compartment-specific biomarker of active microenvironmental remodeling: evidence from bone repair, aging, inflammation, and cancer.Frontiers in medicine · 2026Review
- 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
- Infection of tumor cells withPNAS nexus · 2024Article
- Oncolytic Viruses in the Era of Omics, Computational Technologies, and Modeling: Thesis, Antithesis, and Synthesis.International journal of molecular sciences · 2023Review
- Triple combination therapy for pancreatic cancer remodels stroma and improves survival.Molecular therapy oncolytics · 2023Article
- esRAGE-expressing oHSV enhances anti-tumor efficacy by inhibition of endothelial cell activation.Molecular therapy oncolytics · 2023Article
- Tumour microenvironment: Modulating effects, challenges, and future perspectives of oncolytic virotherapy in Astrocytoma treatment.Annals of medicine and surgery (2012) · 2022Article
- 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
- Systems neuroimmunology: a review of multiomics methodologies to characterize neuroimmunological interactions in spinal and cranial diseases.Neurosurgical focus · 2022Review
- Chimeric Antigen Receptor (CAR) T Cell Therapy for Glioblastoma.Cancer treatment and research · 2022Review
- Herpes simplex virus 1 as an oncolytic viral therapy for refractory cancers.Frontiers in oncology · 2022Review
- Modular network mechanism of CCN1-associated resistance to HSV-1-derived oncolytic immunovirotherapies for glioblastomas.Scientific reports · 2021Article
- Differentiated glioblastoma cells accelerate tumor progression by shaping the tumor microenvironment via CCN1-mediated macrophage infiltration.Acta neuropathologica communications · 2021Article
- Synthetic and systems biology principles in the design of programmable oncolytic virus immunotherapies for glioblastoma.Neurosurgical focus · 2021Review
- The Current State of Oncolytic Herpes Simplex Virus for Glioblastoma Treatment.Oncolytic virotherapy · 2021Review
- Advances and potential pitfalls of oncolytic viruses expressing immunomodulatory transgene therapy for malignant gliomas.Cell death & disease · 2020Review
- YAP Non-cell-autonomously Promotes Pluripotency Induction in Mouse Cells.Stem cell reports · 2020Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Oncolytic viral therapy has been explored widely as an option for glioma treatment but its effectiveness has remained limited. Cysteine rich 61 (CCN1) is an extracellular matrix (ECM) protein elevated in cancer cells that modulates their adhesion and migration by binding cell surface receptors. In this study, we examined a hypothesized role for CCN1 in limiting the efficacy of oncolytic viral therapy for glioma, based on evidence of CCN1 induction that occurs in this setting. Strikingly, we found that exogenous CCN1 in glioma ECM orchestrated a cellular antiviral response that reduced viral replication and limited cytolytic efficacy. Gene expression profiling and real-time PCR analysis revealed a significant induction of type-I interferon responsive genes in response to CCN1 exposure. This induction was accompanied by activation of the Jak/Stat signaling pathway, consistent with induction of an innate antiviral cellular response. Both effects were mediated by the binding of CCN1 to the cell surface integrin α6β1, activating its signaling and leading to rapid secretion of interferon-α, which was essential for the innate antiviral effect. Together, our findings reveal how an integrin signaling pathway mediates activation of a type-I antiviral interferon response that can limit the efficacy of oncolytic viral therapy. Furthermore, they suggest therapeutic interventions to inhibit CCN1-integrin α6 interactions to sensitize gliomas to viral oncolysis.
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What OpenQuestion holds
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.