Journal
JOURNAL OF CELL SCIENCE
Volume 125, Issue 15, Pages 3661-3670Publisher
COMPANY BIOLOGISTS LTD
DOI: 10.1242/jcs.103861
Keywords
Cell migration; Cell-cell adhesion; N-cadherin; 3D matrix; EMT
Categories
Funding
- Beckman Young Investigator Award
- Hellman Family New Faculty Award
- National Institutes of Health EUREKA [GM094798]
- University of California Cancer Research Coordinating Committee
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Cancer cells that originate from epithelial tissues typically lose epithelial specific cell-cell junctions, but these transformed cells are not devoid of cell-cell adhesion proteins. Using hepatocyte-growth-factor-treated MDCK cells that underwent a complete epithelial-to-mesenchymal transition, we analyzed cell-cell adhesion between these highly invasive transformed epithelial cells in a three-dimensional (3D) collagen matrix. In a 3D matrix, these transformed cells formed elongated multicellular chains, and migrated faster and more persistently than single cells in isolation. In addition, the cell clusters were enriched with stress-fiber-like actin bundles that provided contractile forces. N-cadherin-knockdown cells failed to form cell-cell junctions or migrate, and the expression of the N-cadherin cytoplasmic or extracellular domain partially rescued the knockdown phenotype. By contrast, the expression of N-cadherina-catenin chimera rescued the knockdown phenotype, but individual cells within the cell clusters were less mobile. Together, our findings suggest that a dynamic N-cadherin and actin linkage is required for efficient 3D collective migration.
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