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Journal of Cell Science, Vol 114, Issue 6 1237-1246, Copyright © 2001 by Company of Biologists

JOURNAL ARTICLES

Mutant cadherin affects epithelial morphogenesis and invasion, but not transformation

ML Troxell, DJ Loftus, WJ Nelson and JA Marrs
Department of Molecular and Cellular Physiology, Beckman Center B109, Stanford University School of Medicine, Stanford, CA 94305-5426, USA. jmarrs@iupui.edu

MDCK cells were engineered to reversibly express mutant E-cadherin protein with a large extracellular deletion. Mutant cadherin overexpression reduced the expression of endogenous E- and K-cadherins in MDCK cells to negligible levels, resulting in decreased cell adhesion. Despite severe impairment of the cadherin adhesion system, cells overexpressing mutant E-cadherin formed fluid-filled cysts in collagen gel cultures and responded to hepatocyte growth factor/scatter factor (HGF/SF) that induced cellular extension formation with a frequency similar to that of control cysts. However, cells were shed from cyst walls into the lumen and into the collagen matrix prior to and during HGF/SF induced tubule extension. Despite the propensity for cell dissociation, MDCK cells lacking cadherin adhesion molecules were not capable of anchorage-independent growth in soft agar and cell proliferation rate was not affected. Thus, cadherin loss does not induce transformation, despite inducing an invasive phenotype, a later stage of tumor progression. These experiments are especially relevant to tumor progression in cells with altered E-cadherin expression, particularly tumor samples with identified E-cadherin extracellular domain genomic mutations.
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