ArticleNeuro-oncology2016
Tumor microenvironment tenascin-C promotes glioblastoma invasion and negatively regulates tumor proliferation.
Article in Neuro-oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
90 citing papers in PubMed, 1 synthesis or guideline pooled it, 148 citations in OpenAlex.
- Efficacy and safety of bevacizumab in the treatment of adult gliomas: a systematic review and meta-analysis.BMJ open · 2021Pooled it
- Review
- Host TLR4 activation by tenascin-C is associated with MMP14-dependent glioma invasion.Frontiers in oncology · 2026Article
- Loss of Fibronectin Fiber Tension in Glioblastoma is Associated with Microvascular Proliferations and Immune Cell Infiltration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Review
- The glioma microenvironment and its impact on antitumor immunity.Neuro-oncology advances · 2025Review
- Review
- Extracellular Vesicles Carrying Tenascin-C are Clinical Biomarkers and Improve Tumor-Derived DNA Analysis in Glioblastoma Patients.ACS nano · 2025Article
- Development of an orthotopic medulloblastoma zebrafish model for rapid drug testing.Neuro-oncology · 2025Article
- Recent Developments in Glioblastoma-On-A-Chip for Advanced Drug Screening Applications.Small (Weinheim an der Bergstrasse, Germany) · 2025Review
- Emerging insights into the immunosuppressive tumor microenvironment and its implications for glioblastoma immunotherapy.Frontiers in immunology · 2025Review
- Recapitulating the immune microenvironment in pediatric brain cancer: preclinical modeling strategies.Frontiers in immunology · 2025Review
- Review
- Collagen VI deposition primes the glioblastoma microenvironment for invasion through mechanostimulation of β-catenin signaling.PNAS nexus · 2024Article
- Glioma actively orchestrate a self-advantageous extracellular matrix to promote recurrence and progression.BMC cancer · 2024Review
- The tumour microenvironment, treatment resistance and recurrence in glioblastoma.Journal of translational medicine · 2024Review
- Single-cell atlas reveals the immunosuppressive microenvironment and Treg cells landscapes in recurrent Glioblastoma.Cancer gene therapy · 2024Article
- Biosensor-Enhanced Organ-on-a-Chip Models for Investigating Glioblastoma Tumor Microenvironment Dynamics.Sensors (Basel, Switzerland) · 2024Review
- The Potential of the Fibronectin Inhibitor Arg-Gly-Asp-Ser in the Development of Therapies for Glioblastoma.International journal of molecular sciences · 2024Article
- Biology of Tenascin C and its Role in Physiology and Pathology.Current medicinal chemistry · 2024Review
30 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundGlioblastoma (GBM) is the most frequent and aggressive primary brain tumor in adults. Recent research on cancer stroma indicates that the brain microenvironment plays a substantial role in tumor malignancy and treatment responses to current antitumor therapy. In this work, we have investigated the effect of alterations in brain tumor extracellular matrix tenascin-C (TNC) on brain tumor growth patterns including proliferation and invasion.
methodsSince intracranial xenografts from patient-derived GBM neurospheres form highly invasive tumors that recapitulate the invasive features demonstrated in human patients diagnosed with GBM, we studied TNC gain-of-function and loss-of function in these GBM neurospheres in vitro and in vivo.
resultsTNC loss-of-function promoted GBM neurosphere cell adhesion and actin cytoskeleton organization. Yet, TNC loss-of-function or exogenous TNC had no effect on GBM neurosphere cell growth in vitro. In animal models, decreased TNC in the tumor microenvironment was accompanied by decreased tumor invasion and increased tumor proliferation, suggesting that TNC regulates the "go-or-grow" phenotypic switch of glioma in vivo. We demonstrated that decreased TNC in the tumor microenvironment modulated behaviors of stromal cells including endothelial cells and microglia, resulting in enlarged tumor blood vessels and activated microglia in tumors. We further demonstrated that tumor cells with decreased TNC expression are sensitive to anti-proliferative treatment in vitro.
conclusionOur findings suggest that detailed understanding of how TNC in the tumor microenvironment influences tumor behavior and the interactions between tumor cells and surrounding nontumor cells will benefit novel combinatory antitumor strategies to treat malignant brain 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.