ArticleMatrix biology : journal of the International Society for Matrix Biology2017
Fibronectin fibrils regulate TGF-β1-induced Epithelial-Mesenchymal Transition.
Article in Matrix biology : journal of the International Society for Matrix Biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed.
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- A tumor microenvironment integrated (TMI) staging system for pancreatic ductal adenocarcinoma based on cancer-associated fibroblast and molecular consensus signatures.Discover oncology · 2026Article
- Long-term cytokine exposure remodels the methylome and transcriptome of recessive dystrophic epidermolysis bullosa keratinocytes - a bioinformatic analysis.Frontiers in cell and developmental biology · 2026Article
- Evaluating the CRP Interactome: Insights into Possible Novel Roles in Cellular Signaling and Tumorigenicity.Current issues in molecular biology · 2025Review
- A novel six-biomarker panel identified from male breast cancer-associated fibroblasts demonstrates prognostic power for prostate tumors.Journal of translational medicine · 2025Article
- Identification and validation of epithelial‑mesenchymal transition‑related genes for diabetic nephropathy by WGCNA and machine learning.Molecular medicine reports · 2025Article
- The functional role of the extracellular matrix in inflammatory bowel disease associated gut fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2025Review
- The atypical KRASMolecular oncology · 2025Article
- An intricate role of Ang II/AT1 in the modulation of monosodium glutamate-induced pulmonary fibrosis by TGF-β/Smad through quercetin.Scientific reports · 2025Article
- Silencing of LncRNA XIST Suppressed Tumor Growth and Metastasis in Papillary Thyroid Carcinoma by Modulating miR-204/FN1 Axis.ACS omega · 2025Article
- Measuring the biomechanical properties of cell-derived fibronectin fibrils.Biomechanics and modeling in mechanobiology · 2025Article
- Fibrotic extracellular matrix preferentially induces a partial Epithelial-Mesenchymal Transition phenotype in a 3-D agent based model of fibrosis.Mathematical biosciences · 2025Article
- A Multicellular Mechanochemical Model to Investigate Tumor Microenvironment Remodeling and Pre-Metastatic Niche Formation.Cellular and molecular bioengineering · 2024Article
- ADAMTS16 drives epithelial-mesenchymal transition and metastasis through a feedback loop upon TGF-β1 activation in lung adenocarcinoma.Cell death & disease · 2024Article
- Role of circular RNAs in preeclampsia (Review).Experimental and therapeutic medicine · 2024Review
- Differentially expressed extracellular matrix genes functionally separate ameloblastoma from odontogenic keratocyst.BMC oral health · 2024Article
- Delivery technologies for therapeutic targeting of fibronectin in autoimmunity and fibrosis applications.Advanced drug delivery reviews · 2024Review
- The Role of FNDC4 in Inflammation and Metabolism for Various Diseases.Aging and disease · 2024Review
7 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors.
Funding
Abstract
Epithelial-Mesenchymal Transition (EMT) is a dynamic process through which epithelial cells transdifferentiate from an epithelial phenotype into a mesenchymal phenotype. Previous studies have demonstrated that both mechanical signaling and soluble growth factor signaling facilitate this process. One possible point of integration for mechanical and growth factor signaling is the extracellular matrix. Here we investigate the role of the extracellular matrix (ECM) protein fibronectin (FN) in this process. We demonstrate that inhibition of FN fibrillogenesis blocks activation of the Transforming Growth Factor-Beta (TGF-β) signaling pathway via Smad2 signaling, decreases cell migration and ultimately leads to inhibition of EMT. Results show that soluble FN, FN fibrils, or increased contractile forces are insufficient to independently induce EMT. We further demonstrate that inhibition of latent TGF-β1 binding to FN fibrils via either a monoclonal blocking antibody against the growth factor binding domain of FN or through use of a FN deletion mutant that lacks the growth factor binding domains of FN blocks EMT progression, indicating a novel role for FN in EMT in which the assembly of FN fibrils serves to localize TGF-β1 signaling to drive EMT.
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Registered trials
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