Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Integrin-dependent actomyosin contraction regulates epithelial cell scattering.

Johan de Rooij1, Andre Kerstens, Gaudenz Danuser

  • 1Department of Cell Biology, The Scripps Research Institute, La Jolla, CA 92037, USA.

The Journal of Cell Biology
|October 12, 2005
PubMed
Summary

Epithelial cell scattering, a process mimicking cancer invasion, is driven by integrin-mediated traction forces. These forces disrupt cell-cell adhesion through actomyosin activity, not by weakening E-cadherin.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Discovery and analytical assessment of urinary miRNA biomarkers for cervical cancer using advanced small RNA sequencing.

Translational oncology·2026
Same author

Modulation of Oncogenic KRAS Signaling by Branched Actin-driven Cell Membrane Protrusions.

Research square·2026
Same author

Volumetric Cyclic Immunofluorescence for 3D Spatial Profiling of Immune Structures in Human FFPE Tissue.

bioRxiv : the preprint server for biology·2026
Same author

Metabolic control of smooth muscle cell phenotype switching in atherosclerosis.

bioRxiv : the preprint server for biology·2026
Same author

RhoG, Rac1 and Cdc42 cooperation in cell protrusion revealed by multiplexed optogenetics and biosensor imaging.

bioRxiv : the preprint server for biology·2026
Same author

Allosteric Biosensors Unravel GTPase-Effector Feedback.

bioRxiv : the preprint server for biology·2026

Area of Science:

  • Cell Biology
  • Biophysics
  • Cancer Research

Background:

  • Epithelial cell scattering in vitro models key processes like cancer invasion and metastasis.
  • This scattering is induced by hepatocyte growth factor (HGF) and involves cadherin junctions.
  • Extracellular matrix (ECM) proteins like collagen and fibronectin enhance scattering, suggesting integrin-cadherin crosstalk.

Purpose of the Study:

  • To investigate the role of integrin-mediated adhesion and ECM interactions in epithelial cell scattering.
  • To determine the contribution of actomyosin-dependent forces to the disruption of cell-cell junctions during scattering.
  • To elucidate the mechanism by which hepatocyte growth factor (HGF) induces cell scattering.

Main Methods:

  • Utilizing Madin-Darby canine kidney cells for in vitro scattering assays.

Related Experiment Videos

  • Employing time-lapse imaging to observe cell behavior during scattering.
  • Manipulating extracellular matrix (ECM) composition and substrate rigidity to assess their effects on scattering.
  • Measuring integrin-mediated adhesion and myosin regulatory light chain phosphorylation.

    • Main Results:

    • HGF did not decrease E-cadherin function but enhanced integrin-mediated adhesion.
    • Cell scattering correlated with increased integrin adhesion and myosin regulatory light chain phosphorylation.
    • Scattering was promoted on rigid substrates generating high traction forces, compared to compliant substrates.
    • Tension on cell-cell junctions appeared to contribute to the disruption of cell-cell adhesion.

    Conclusions:

    • Integrin-dependent actomyosin traction force is the primary mediator of cell-cell adhesion disruption during epithelial cell scattering.
    • The findings highlight the mechanical forces governing cell-cell junction stability and cell motility.
    • This study provides insights into the biophysical mechanisms underlying epithelial-mesenchymal transitions and cancer metastasis.