ArticleCancer science2009
Endogenous tenascin-C enhances glioblastoma invasion with reactive change of surrounding brain tissue.
Article in Cancer science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Systematic review of protein biomarkers of invasive behavior in glioblastoma.Molecular neurobiology · 2014Pooled it
- Oct-4+/Tenascin C+ neuroblastoma cells serve as progenitors of tumor-derived endothelial cells.Cell research · 2011Trial
- Review
- The Extracellular Matrix, the Silent 'Architect' of Glioma.Biomedicines · 2026Review
- Host TLR4 activation by tenascin-C is associated with MMP14-dependent glioma invasion.Frontiers in oncology · 2026Article
- MiR-7 inhibits progression of glioblastoma by impairing autophagy resolution, energy metabolism and ECM remodeling.Journal of experimental & clinical cancer research : CR · 2025Article
- Biosensor-Enhanced Organ-on-a-Chip Models for Investigating Glioblastoma Tumor Microenvironment Dynamics.Sensors (Basel, Switzerland) · 2024Review
- Substrate-bound and soluble domains of tenascin-C regulate differentiation, proliferation and migration of neural stem and progenitor cells.Frontiers in cellular neuroscience · 2024Article
- Glioblastoma Microenvironment and Invasiveness: New Insights and Therapeutic Targets.International journal of molecular sciences · 2023Review
- Review
- Optimal managements of elderly patients with glioblastoma.Japanese journal of clinical oncology · 2022Review
- Glycomaterials to Investigate the Functional Role of Aberrant Glycosylation in Glioblastoma.Advanced healthcare materials · 2022Review
- Matricellular protein tenascin C: Implications in glioma progression, gliomagenesis, and treatment.Frontiers in oncology · 2022Review
- Involvement of Integrin-Activating Peptides Derived from Tenascin-C in Cancer Aggression and New Anticancer Strategy Using the Fibronectin-Derived Integrin-Inactivating Peptide.Molecules (Basel, Switzerland) · 2020Review
- Biologically Active TNIIIA2 Region in Tenascin-C Molecule: A Major Contributor to Elicit Aggressive Malignant Phenotypes From Tumors/Tumor Stroma.Frontiers in immunology · 2020Review
- Pleiotropic Role of Tenascin-C in Central Nervous System Diseases: From Basic to Clinical Applications.Frontiers in neurology · 2020Review
- IL-33/ST2 axis promotes glioblastoma cell invasion by accumulating tenascin-C.Scientific reports · 2019Article
- Quantitative proteomic profiling of tumor-associated vascular endothelial cells in colorectal cancer.Biology open · 2019Article
- The Cytoskeleton-A Complex Interacting Meshwork.Cells · 2019Review
- Tenascin-C expression is significantly associated with the progression and prognosis in gastric GISTs.Medicine · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tenascin-C is an extracellular matrix glycoprotein implicated in embryogenesis, wound healing and tumor progression. We previously revealed that tenascin-C expression is correlated with the prognosis of patients with glioblastoma. However, the exact role of endogenous tenascin-C in regulation of glioblastoma proliferation and invasion remains to be established. We show here that endogenous tenascin-C facilitates glioblastoma invasion, followed by reactive change of the surrounding brain tissue. Although shRNA-mediated knockdown of endogenous tenascin-C does not affect proliferation of glioblastoma cells, it abolishes cell migration on a two-dimensional substrate and tumor invasion with brain tissue changes in a xenograft model. The tyrosine phosphorylation of focal adhesion kinase, a cytoplasmic tyrosine kinase that associates with integrins, was decreased in tenascin-C-knockdown cells. In the analysis of clinical samples, tenascin-C expression correlates with the volume of peritumoral reactive change detected by magnetic resonance imaging. Interestingly, glioblastoma cells with high tenascin-C expression infiltrate brain tissue in an autocrine manner. Our results suggest that endogenous tenascin-C contributes the invasive nature of glioblastoma and the compositional change of brain tissue, which renders tenascin-C as a prime candidate for anti-invasion therapy for glioblastoma.
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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.