ArticleOncogene2003
Tenascin-C blocks cell-cycle progression of anchorage-dependent fibroblasts on fibronectin through inhibition of syndecan-4.
Article in Oncogene, 2003. 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, 85 citations in OpenAlex.
- SDC4 silencing promotes cell cycle arrest at the restriction point (R point) in anoikis-resistant endothelial cells.Cytotechnology · 2026Article
- Fibronectin is required for proper extracellular matrix organization and cardiac outflow tract elongation inFrontiers in cell and developmental biology · 2026Article
- Deciphering the Tenascin-C Nexus: A Comprehensive Review of Its Involvement in Chronic Respiratory Diseases.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025Review
- Mesodermal fibronectin controls cell shape, polarity, and mechanotransduction in the second heart field during cardiac outflow tract development.Developmental cell · 2025Article
- Shaping Oncogenic Microenvironments: Contribution of Fibronectin.Frontiers in cell and developmental biology · 2024Review
- Article
- The extracellular matrix molecule tenascin-C modulates cell cycle progression and motility of adult neural stem/progenitor cells from the subependymal zone.Cellular and molecular life sciences : CMLS · 2022Article
- The jam session between muscle stem cells and the extracellular matrix in the tissue microenvironment.NPJ Regenerative medicine · 2022Review
- Tenascin-C fibronectin D domain is involved in the fine-tuning of glial response to CNS injuryFrontiers in cell and developmental biology · 2022Article
- LOXL3 Silencing Affected Cell Adhesion and Invasion in U87MG Glioma Cells.International journal of molecular sciences · 2021Article
- Effects of Tenascin C on the Integrity of Extracellular Matrix and Skin Aging.International journal of molecular sciences · 2020Article
- Elevated glucose alters global gene expression and tenascin-C alternative splicing in mesangial cells.Matrix biology plus · 2020Article
- Expression Changes and Impact of the Extracellular Matrix on Etoposide Resistant Human Retinoblastoma Cell Lines.International journal of molecular sciences · 2020Article
- Tenascin-C deficiency impairs alveolarization and microvascular maturation during postnatal lung development.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Article
- Biologically Active TNIIIA2 Region in Tenascin-C Molecule: A Major Contributor to Elicit Aggressive Malignant Phenotypes From Tumors/Tumor Stroma.Frontiers in immunology · 2020Review
- Down-regulation of tenascin-C inhibits breast cancer cells development by cell growth, migration, and adhesion impairment.PloS one · 2020Article
- Co-cultured Bone-marrow Derived and Tendon Stem Cells: Novel Seed Cells for Bone Regeneration.Open life sciences · 2019Article
- Tenascin-C Promotes Tumor Cell Migration and Metastasis through Integrin α9β1-Mediated YAP Inhibition.Cancer research · 2018Article
- Counterbalancing anti-adhesive effects of Tenascin-C through fibronectin expression in endothelial cells.Scientific reports · 2017Article
- αV-class integrins exert dual roles on α5β1 integrins to strengthen adhesion to fibronectin.Nature communications · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tenascin-C is an adhesion-modulatory extracellular matrix protein that is predominantly expressed during embryonic development, wound healing and in tumor stroma. Here we report that anchorage-dependent human, rat and mouse fibroblasts adhere poorly and fail to proliferate on pure tenascin-C. This was due to a significant reduction of cyclin-dependent kinase 2 (cdk2) activity, resulting from elevated expression and association of the cdk inhibitors (CKIs) p21Cip1 and p27Kip1. To analyse the effect of tenascin-C on fibronectin-mediated adhesion, cells were plated on a mixed fibronectin/tenascin-C substratum. Compared to fibronectin alone, cell spreading and adhesion signaling were compromised, as determined by delayed phosphorylation kinetics of focal adhesion kinase (FAK). Despite the presence of growth factors, these cells remained arrested in the G1 phase of the cell cycle. In contrast to cells plated on pure tenascin-C, cdk2 activity appeared to be inhibited independently of CKIs. Interestingly, overexpression of the transmembrane proteoglycan syndecan-4 restored cell spreading, adhesion signaling and DNA replication on the fibronectin/tenascin-C substratum. A similar rescue was observed using a recombinant peptide that spans the syndecan-4-binding site in fibronectin. This indicates that tenascin-C causes cell cycle arrest and cdk2 inactivation by interfering with fibronectin-syndecan-4 interactions. We therefore propose that syndecan-4 signaling plays a central role in the control of cellular proliferation of anchorage-dependent fibroblasts.
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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.