ArticleThe American journal of pathology2003
Involvement of large tenascin-C splice variants in breast cancer progression.
Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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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
49 citing papers in PubMed.
- Pro-Apoptotic and Anti-EMT Activity of Wild Ginseng Adventitious Root Extract in MDA-MB-231 TNBC Cells: Association with GSK-3β/β-Catenin Signaling.Pharmaceuticals (Basel, Switzerland) · 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
- NAT10 promotes gastric cancer progression by enhancing the N4-acetylcytidine modification of TNC mRNA.Infectious agents and cancer · 2025Article
- Article
- Biology of Tenascin C and its Role in Physiology and Pathology.Current medicinal chemistry · 2024Review
- Extracellular matrix complexity in biomarker studies: a novel assay detecting total serum tenascin-C reveals different distribution to isoform-specific assays.Frontiers in immunology · 2023Article
- Dual Role of Fibroblasts Educated by Tumour in Cancer Behavior and Therapeutic Perspectives.International journal of molecular sciences · 2022Review
- The Role of Extracellular Matrix Proteins in Breast Cancer.Journal of clinical medicine · 2022Review
- Review
- Identification of Significant Genes and Pathways Associated with Tenascin-C in Cancer Progression by Bioinformatics Analysis.Advanced biomedical research · 2022Article
- A functional network of gastric-cancer-associated splicing events controlled by dysregulated splicing factors.NAR genomics and bioinformatics · 2020Article
- Tumor suppressor genes and allele-specific expression: mechanisms and significance.Oncotarget · 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
- Phage display screening of therapeutic peptide for cancer targeting and therapy.Protein & cell · 2019Review
- The Promoting Effect of the Extracellular Matrix Peptide TNIIIA2 Derived from Tenascin-C in Colon Cancer Cell Infiltration.International journal of molecular sciences · 2017Article
- Splicing imbalances in basal-like breast cancer underpin perturbation of cell surface and oncogenic pathways and are associated with patients' survival.Scientific reports · 2017Article
- Aberrant RNA splicing in cancer; expression changes and driver mutations of splicing factor genes.Oncogene · 2016Review
- Article
- Article
- Role of tenascins in the ECM of gliomas.Cell adhesion & migration · 2015Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alternative splicing of fibronectin-like type III (FNIII) repeats of tenascin-C (Tn-C) generates a number of splice variants. The distribution of large variants, typical components of provisional extracellular matrices that are up-regulated during tumor stroma remodeling, was here studied by immunoblotting and immunohistochemistry using a monoclonal antibody against the FNIII B domain (named 4C8MS) in a series of human breast cancers. Large Tn-C variants were found at only low levels in normal breast tissues, but were highly expressed at invading sites of intraductal cancers and in the stroma of invasive ductal cancers, especially at invasion fronts. There was a positive correlation between the expression of large Tn-C variants and the cell proliferation rate determined by immunolabeling of the Ki-67 antigen. Of the Tn-C recombinant fragments (all FNIII repeats or mFNIII FL, the conserved FNIII domain only, the epidermal growth factor-like domain, and the fibrinogen-like domain) which were expressed by CHO-K1 cells transfected with mouse Tn-C cDNAs, only the mFNIII FL enhanced in vitro migration and mitotic activity of mammary cancer cells derived from a Tn-C-null mouse. Addition of 4C8MS blocked the function of mFNIII FL. These findings provide strong evidence that the FNIII alternatively spliced region has important roles in tumor progression of breast cancer.
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