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¹ Department of Cell Biology, The Scripps Research Institute, La Jolla, CA 92037
² Department of Microbiology, Cardiovascular Research Center, Mellon Prostate Cancer Institute, University of Virginia, Charlottesville, VA 22908
³ Department of Biomedical Engineering, Cardiovascular Research Center, Mellon Prostate Cancer Institute, University of Virginia, Charlottesville, VA 22908

Correspondence to Johan de Rooij: j.d.rooij{at}nki.nl

The scattering of Madin-Darby canine kidney cells in vitro mimics key aspects of epithelial–mesenchymal transitions during development, carcinoma cell invasion, and metastasis. Scattering is induced by hepatocyte growth factor (HGF) and is thought to involve disruption of cadherin-dependent cell–cell junctions. Scattering is enhanced on collagen and fibronectin, as compared with laminin1, suggesting possible cross talk between integrins and cell–cell junctions. We show that HGF does not trigger any detectable decrease in E-cadherin function, but increases integrin-mediated adhesion. Time-lapse imaging suggests that tension on cell–cell junctions may disrupt cell–cell adhesion. Varying the density and type of extracellular matrix proteins shows that scattering correlates with stronger integrin adhesion and increased phosphorylation of the myosin regulatory light chain. To directly test the role of integrin-dependent traction forces, substrate compliance was varied. Rigid substrates that produce high traction forces promoted scattering, in comparison to more compliant substrates. We conclude that integrin-dependent actomyosin traction force mediates the disruption of cell–cell adhesion during epithelial cell scattering.

M.A. Schwartz and C.M. Waterman-Storer contributed equally to this paper.

J. de Rooij's present address is Dept. of Cell Biology, Netherlands Cancer Institute, 1066 CX Amsterdam, Netherlands.

A. Kersten's present address is University of Texas at El Paso, College of Engineering, El Paso, TX 79968.

Abbreviations used in this paper: 2D, two-dimensional; CCD, charge-coupled device; Cn, collagen; EMT, epithelial–mesenchymal transition; Fn, fibronectin; HGF, hepatocyte growth factor; Ln, laminin; MLC, myosin II regulatory light chain; Vn, vitronectin; ZO-1, zona-occludens-1.

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