ArticleMolecular biology of the cell2007
E-cadherin homophilic ligation inhibits cell growth and epidermal growth factor receptor signaling independently of other cell interactions.
Article in Molecular biology of the cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 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.
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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
125 citing papers in PubMed, 219 citations in OpenAlex.
- A cascade via CD276/PI3K/SIRT1/E-Cad in overcoming contact inhibition of proliferation in hepatocellular carcinoma cells.Molecular and clinical oncology · 2026Article
- Epidermal growth factor receptor is an essential component in E-cadherin force transduction complexes.Journal of cell science · 2025Article
- Emerging functions of Plakophilin 4 in the control of cell contact dynamics.Cell communication and signaling : CCS · 2025Review
- Review
- Development and dysfunction of structural cells in eosinophilic esophagitis.The Journal of allergy and clinical immunology · 2024Review
- Reversible Photoregulation of Cell-Cell Adhesions With Opto-E-cadherin.Bio-protocol · 2024Article
- Afadin-nectin forces its way to the front.The Journal of cell biology · 2024Article
- Role of trefoil factors in maintaining gut health in food animals.Frontiers in veterinary science · 2024Review
- Reversible photoregulation of cell-cell adhesions with opto-E-cadherin.Nature communications · 2023Article
- Interplay between EGFR, E-cadherin, and PTP1B in epidermal homeostasis.Tissue barriers · 2023Review
- Sustained postconfluent culture of human mammary epithelial cells enriches for luminal and c-Kit+ subtypes.Breast cancer research : BCR · 2023Article
- Cadherins and catenins in cancer: connecting cancer pathways and tumor microenvironment.Frontiers in cell and developmental biology · 2023Review
- The Regulation of the Hippo Pathway by Intercellular Junction Proteins.Life (Basel, Switzerland) · 2022Review
- Dual role of E-cadherin in cancer cells.Tissue barriers · 2022Review
- Activation of CD44 signaling in leader cells induced by tumor-associated macrophages drives collective detachment in luminal breast carcinomas.Cell death & disease · 2022Article
- Invadopodia play a role in prostate cancer progression.BMC cancer · 2022Article
- Establishment of bovine 3D enteroid-derived 2D monolayers.Veterinary research · 2022Article
- A Double-Negative Feedback Interaction between miR-21 and PPAR-α in Clear Renal Cell Carcinoma.Cancers · 2022Article
- Mechanical disruption of E-cadherin complexes with epidermal growth factor receptor actuates growth factor-dependent signaling.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Article
65 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
E-cadherin function leads to the density-dependent contact inhibition of cell growth. Because cadherins control the overall state of cell contact, cytoskeletal organization, and the establishment of many other kinds of cell interactions, it remains unknown whether E-cadherin directly transduces growth inhibitory signals. To address this question, we have selectively formed E-cadherin homophilic bonds at the cell surface of isolated epithelial cells by using functionally active recombinant E-cadherin protein attached to microspheres. We find that E-cadherin ligation alone reduces the frequency of cells entering the S phase, demonstrating that E-cadherin ligation directly transduces growth inhibitory signals. E-cadherin binding to beta-catenin is required for cell growth inhibition, but beta-catenin/T-cell factor transcriptional activity is not involved in growth inhibition resulting from homophilic binding. Neither E-cadherin binding to p120-catenin nor beta-catenin binding to alpha-catenin, and thereby the actin cytoskeleton, is required for growth inhibition. E-cadherin ligation also inhibits epidermal growth factor (EGF) receptor-mediated growth signaling by a beta-catenin-dependent mechanism. It does not affect EGF receptor autophosphorylation or activation of ERK, but it inhibits transphosphorylation of Tyr845 and activation of signal transducers and activators of transcription 5. Thus, E-cadherin homophilic binding independent of other cell contacts directly transduces growth inhibition by a beta-catenin-dependent mechanism that inhibits selective signaling functions of growth factor receptors.
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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.