ArticleCells2024
Actin Cytoskeleton Remodeling Accompanied by Redistribution of Adhesion Proteins Drives Migration of Cells in Different EMT States.
Article in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Paratuberculosis vaccination induces a phenotype consistent with trained immunity in bovine neutrophils.NPJ vaccines · 2026Article
- ViMST: vision transformer-based dual modality multi-task graph contrastive network for spatial transcriptomics microenvironments investigation.BMC biology · 2026Article
- Venous Nanoflap Oscillations: Biomechanical Determinants and Hydrodynamic Consequences in the Deep Cerebral Venous System.International journal of molecular sciences · 2026Review
- Protocadherin 1 (PCDH1) Promotes Pancreatic Cancer Metastasis by Regulating Epithelial-Mesenchymal Transition (EMT) Progression Through the NF-κB Pathway.Cancer management and research · 2026Article
- The involvement of circular RNAs in breast cancer metastasis: Insight into EMT-related signaling pathways.BioImpacts : BI · 2026Review
- Comparison of viscoelastic properties of breast cancer and normal cells using AFM, FLIM and ToF-SIMS techniques.Scientific reports · 2025Article
- A fibroblast-specific gene signature as a therapeutic target for glioblastoma developed based on the characteristics of tumor microenvironment.European journal of medical research · 2025Article
- Connexin Restrains EMT by Dual-Domain Mechanisms to Preserve Epithelial Identity.Research square · 2025Article
- Epithelial-Mesenchymal Transition Increases the Susceptibility of Human A549 Cells to Nanosecond Pulsed Electric Fields.International journal of molecular sciences · 2025Article
- Endometrial E-cadherin and N-cadherin Expression during the Mid-Secretory Phase of Women with Ovarian Endometrioma or Uterine Fibroids.Journal of personalized medicine · 2024Article
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Authors and funding
5 authors.
Funding
Abstract
Epithelial-mesenchymal transition (EMT) is a process during which epithelial cells lose epithelial characteristics and gain mesenchymal features. Here, we used several cell models to study migratory activity and redistribution of cell-cell adhesion proteins in cells in different EMT states: EGF-induced EMT of epithelial IAR-20 cells; IAR-6-1 cells with a hybrid epithelial-mesenchymal phenotype; and their more mesenchymal derivatives, IAR-6-1-DNE cells lacking adherens junctions. In migrating cells, the cell-cell adhesion protein α-catenin accumulated at the leading edges along with ArpC2/p34 and α-actinin. Suppression of α-catenin shifted cell morphology from fibroblast-like to discoid and attenuated cell migration. Expression of exogenous α-catenin in MDA-MB-468 cells devoid of α-catenin drastically increased their migratory capabilities. The Y654 phosphorylated form of β-catenin was detected at integrin adhesion complexes (IACs). Co-immunoprecipitation studies indicated that α-catenin and pY654-β-catenin were associated with IAC proteins: vinculin, zyxin, and α-actinin. Taken together, these data suggest that in cells undergoing EMT, catenins not participating in assembly of adherens junctions may affect cell migration.
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