ArticleScientific reports2017
Actomyosin contractility provokes contact inhibition in E-cadherin-ligated keratinocytes.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 43 citations in OpenAlex.
- Mechanobiology of the Hippo-YAP Signaling Network.Cold Spring Harbor perspectives in biology · 2026Article
- The therapeutic potential of high-intensity interval training in a breast cancer model: focus on the Hippo signaling pathway.Breast cancer (Tokyo, Japan) · 2025Article
- Keratinocyte Capability for Smooth Sheet Formation on a Step Pattern Substrate.Bioengineering (Basel, Switzerland) · 2025Article
- Hippo Pathway Regulates Cell Proliferation in Skin Epidermis Exposed to Mechanical Forces.Journal of cellular and molecular medicine · 2025Article
- Double-sided niche regulation in skin stem cell and cancer: mechanisms and clinical applications.Molecular cancer · 2025Review
- YAP/TAZ Signalling Controls Epidermal Keratinocyte Fate.International journal of molecular sciences · 2024Review
- Plakophilin 4 controls the spatio-temporal activity of RhoA at adherens junctions to promote cortical actin ring formation and tissue tension.Cellular and molecular life sciences : CMLS · 2024Article
- Tankyrase inhibition interferes with junction remodeling, induces leakiness, and disturbs YAP1/TAZ signaling in the endothelium.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Volume-regulated anion channels conduct ATP in undifferentiated mammary cells and promote tumorigenesis in xenograft nude mouse.Frontiers in cell and developmental biology · 2024Article
- Collective heterogeneity of mitochondrial potential in contact inhibition of proliferation.Biophysical journal · 2023Article
- EPLINβ Is Involved in the Assembly of Cadherin-catenin Complexes in Osteoblasts and Affects Bone Formation.Acta histochemica et cytochemica · 2022Article
- Local contractions regulate E-cadherin rigidity sensing.Science advances · 2022Article
- Sphingosine-1-Phosphate Induces ATP Release via Volume-Regulated Anion Channels in Breast Cell Lines.Life (Basel, Switzerland) · 2021Article
- MAGI1 inhibits the AMOTL2/p38 stress pathway and prevents luminal breast tumorigenesis.Scientific reports · 2021Article
- Anti-Malignant Effect of Tensile Loading to Adherens Junctions in Cutaneous Squamous Cell Carcinoma Cells.Frontiers in cell and developmental biology · 2021Article
- Lamin-Related Congenital Muscular Dystrophy Alters Mechanical Signaling and Skeletal Muscle Growth.International journal of molecular sciences · 2020Article
- Coordination between Cell Motility and Cell Cycle Progression in Keratinocyte Sheets via Cell-Cell Adhesion and Rac1.iScience · 2020Article
- Hippo-Yap/Taz signaling: Complex network interactions and impact in epithelial cell behavior.Wiley interdisciplinary reviews. Developmental biology · 2020Review
- Cell mechanosensing underlies homeostasis of multicellular systems.Biophysics and physicobiology · 2020Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Confluence-dependent inhibition of epithelial cell proliferation, termed contact inhibition, is crucial for epithelial homeostasis and organ size control. Here we report that among epithelial cells, keratinocytes, which compose the stratified epithelium in the skin, possess a unique, actomyosin-dependent mechanism for contact inhibition. We have observed that under actomyosin-inhibited conditions, cell-cell contact itself through E-cadherin promotes proliferation of keratinocytes. Actomyosin activity in confluent keratinocytes, however, inhibits nuclear localization of β-catenin and YAP, and causes attenuation of β-catenin- and YAP-driven cell proliferation. Confluent keratinocytes develop E-cadherin-mediated punctate adhesion complexes, to which radial actin cables are connected. Eliminating the actin-to-E-cadherin linkage by depleting α-catenin increases proliferation of confluent keratinocytes. By contrast, enforced activation of RhoA-regulated actomyosin or external application of pulling force to ligated E-cadherin attenuates their proliferation, suggesting that tensile stress at E-cadherin-mediated adhesion complexes inhibits proliferation of confluent keratinocytes. Our results highlight actomyosin contractility as a crucial factor that provokes confluence-dependent inhibition of keratinocyte proliferation.
Indexed as
Identifiers
What OpenQuestion holds
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.