ArticleOncogene2014
Mammary epithelial cell interactions with fibronectin stimulate epithelial-mesenchymal transition.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 papers.
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Who cites it
148 citing papers in PubMed, 241 citations in OpenAlex.
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- Decellularized extracellular matrix restores Fibronectin/Integrin β1 balance through extracellular vesicles to rejuvenate chondrocytes and alleviate osteoarthritis progression.Journal of orthopaedic translation · 2026Article
- Integrin-Piezo1 Axis Drives ECM Remodeling and Invasion of 3D Breast Epithelium.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The FN1-ITGB4 Axis Drives Acquired Chemoresistance in Bladder Cancer by Activating FAK Signaling.Oncology research · 2026Article
- Matrix Stiffness Regulates TGFβ1-Induced αSMA Expression via a G9a-LATS-YAP Signaling Cascade.FASEB bioAdvances · 2025Article
- Progenitor Cell Dynamics in Androgenetic Alopecia: Insights from Spatially Resolved Transcriptomics.International journal of molecular sciences · 2025Article
- Transforming Cancer Therapy: Unlocking the Potential of Targeting Vascular and Stromal Cells in the Tumor Microenvironment.Cancer research · 2025Review
- β-catenin as a key regulator of the cisplatin response in tumor cells.Clinical and experimental medicine · 2025Review
- Tumor budding and poorly differentiated clusters as a biological continuum in colorectal cancer invasion and prognosis.Scientific reports · 2025Article
- A Review on Bioengineering the Bovine Mammary Gland: The Role of the Extracellular Matrix and Reconstruction Prospects.Bioengineering (Basel, Switzerland) · 2025Review
- Exploring the role of EMT in ovarian cancer progression using a multiscale mathematical model.NPJ systems biology and applications · 2025Article
- STModule: identifying tissue modules to uncover spatial components and characteristics of transcriptomic landscapes.Genome medicine · 2025Article
- Harnessing the tumor microenvironment: targeted cancer therapies through modulation of epithelial-mesenchymal transition.Journal of hematology & oncology · 2025Review
- Cepharanthine may inhibit the proliferation of prostate cells by blocking the EGFR/PI3K/AKT signaling pathway: comprehensive network analysis, molecular docking, and experimental evaluation.Frontiers in pharmacology · 2025Article
- Regulation of Cancer Stem Cells in the Tumor Microenvironment.Cancer heterogeneity and plasticity · 2025Article
- Consequences of platelet-educated cancer cells on the expression of inflammatory and metastatic glycoproteins.PloS one · 2025Article
- Understanding the cellular dynamics, engineering perspectives and translation prospects in bioprinting epithelial tissues.Bioactive materials · 2025Review
- Differentially expressed extracellular matrix genes functionally separate ameloblastoma from odontogenic keratocyst.BMC oral health · 2024Article
- STIE: Single-cell level deconvolution, convolution, and clustering in in situ capturing-based spatial transcriptomics.Nature communications · 2024Article
88 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In the mammary gland, the stromal extracellular matrix (ECM) undergoes dramatic changes during development and in tumorigenesis. For example, normal adult breast tissue is largely devoid of the ECM protein fibronectin (FN) whereas high FN levels have been detected in the stroma of breast tumors. FN is an established marker for epithelial-mesenchymal transition (EMT), which occurs during development and has been linked to cancer. During EMT, epithelial cell adhesion switches from cell-cell contacts to mainly cell-ECM interactions, raising the possibility that FN may have a role in promoting this transition. Using MCF-10A mammary epithelial cells, we show that exposure to exogenous FN induces an EMT response including upregulation of the EMT markers FN, Snail, N-cadherin, vimentin, the matrix metalloprotease MMP2, α-smooth muscle actin and phospho-Smad2, as well as acquisition of cell migratory behavior. FN-induced EMT depends on Src kinase and extracellular signal-regulated kinase/mitogen-activated protein (ERK/MAP) kinase signaling but not on the immediate early gene EGR-1. FN initiates EMT under serum-free conditions; this response is partially reversed by a transforming growth factor (TGF)β-neutralizing antibody, suggesting that FN enhances the effect of endogenous TGFβ. EMT marker expression is upregulated in cells on a fragment of FN containing the integrin-binding domain but not other domains. Differences in gene expression between FN and Matrigel are maintained with addition of a subthreshold level of TGFβ1. Together, these results show that cells interacting with FN are primed to respond to TGFβ. The ability of FN to induce EMT shows an active role for the stromal ECM in this process and supports the notion that the increased levels of FN observed in breast tumors facilitate tumorigenesis.
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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.