ArticlePloS one2010
Differential regulation of growth-promoting signalling pathways by E-cadherin.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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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Who cites it
16 citing papers in PubMed, 33 citations in OpenAlex.
- Interplay between EGFR, E-cadherin, and PTP1B in epidermal homeostasis.Tissue barriers · 2023Review
- Introducing Circulating Vasculature-Related Transcripts as Biomarkers in Coronary Artery Disease.Molecular diagnosis & therapy · 2023Article
- E-Cadherin Signaling in Salivary Gland Development and Autoimmunity.Journal of clinical medicine · 2022Review
- FSH Levels Are Related to E-cadherin Expression and Subcellular Location in Nonfunctioning Pituitary Tumors.The Journal of clinical endocrinology and metabolism · 2020Article
- An overview of technical considerations for Western blotting applications to physiological research.Scandinavian journal of medicine & science in sports · 2017Review
- Characterization and classification of adherent cells in monolayer culture using automated tracking and evolutionary algorithms.Bio Systems · 2016Article
- Sources of variability in cytosolic calcium transients triggered by stimulation of homogeneous uro-epithelial cell monolayers.Journal of the Royal Society, Interface · 2015Article
- From cell membrane to the nucleus: an emerging role of E-cadherin in gene transcriptional regulation.Journal of cellular and molecular medicine · 2014Review
- A novel bidirectional positive-feedback loop between Wnt-β-catenin and EGFR-ERK plays a role in context-specific modulation of epithelial tissue regeneration.Journal of cell science · 2014Article
- Epigenetic modulation of signal transduction pathways in HPV-associated HNSCC.Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · 2013Article
- Urothelial signaling.Physiological reviews · 2013Review
- The modulatory effect of cell–cell contact on the tumourigenic potential of pre-malignant epithelial cells: a computational exploration.Journal of the Royal Society, Interface · 2013Article
- Indometacin ameliorates high glucose-induced proliferation and invasion via modulation of e-cadherin in pancreatic cancer cells.Current medicinal chemistry · 2013Article
- Spherical bullet formation via E-cadherin promotes therapeutic potency of mesenchymal stem cells derived from human umbilical cord blood for myocardial infarction.Molecular therapy : the journal of the American Society of Gene Therapy · 2012Article
- Significance of epithelial growth factor in the epithelial-mesenchymal transition of human gallbladder cancer cells.Cancer science · 2012Article
- High glucose promotes pancreatic cancer cell proliferation via the induction of EGF expression and transactivation of EGFR.PloS one · 2011Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDespite the well-documented association between loss of E-cadherin and carcinogenesis, as well as the link between restoration of its expression and suppression of proliferation in carcinoma cells, the ability of E-cadherin to modulate growth-promoting cell signalling in normal epithelial cells is less well understood and frequently contradictory. The potential for E-cadherin to co-ordinate different proliferation-associated signalling pathways has yet to be fully explored. METHODOLOGY/PRINCIPAL
findingsUsing a normal human urothelial (NHU) cell culture system and following a calcium-switch approach, we demonstrate that the stability of NHU cell-cell contacts differentially regulates the Epidermal Growth Factor Receptor (EGFR)/Extracellular Signal-Regulated Kinase (ERK) and Phosphatidylinositol 3-Kinase (PI3-K)/AKT pathways. We show that stable cell contacts down-modulate the EGFR/ERK pathway, whilst inducing PI3-K/AKT activity, which transiently enhances cell growth at low density. Functional inactivation of E-cadherin interferes with the capacity of NHU cells to form stable calcium-mediated contacts, attenuates E-cadherin-mediated PI3-K/AKT induction and enhances NHU cell proliferation by allowing de-repression of the EGFR/ERK pathway and constitutive activation of β-catenin-TCF signalling. CONCLUSIONS/SIGNIFICANCE: Our findings provide evidence that E-cadherin can differentially and concurrently regulate specific growth-related signalling pathways in a context-specific fashion, with direct, functional consequences for cell proliferation and population growth. Our observations not only reveal a novel, complex role for E-cadherin in normal epithelial cell homeostasis and tissue regeneration, but also provide the basis for a more complete understanding of the consequences of E-cadherin loss on malignant transformation.
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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.