E-cadherin expression during the acidic FGF-induced dispersion of a rat bladder carcinoma cell line

Exp Cell Res. 1992 Aug;201(2):347-57. doi: 10.1016/0014-4827(92)90283-e.


Cell dissociation and acquisition of cell motility are major events in morphogenesis, wound repair, and cancer invasion and metastasis. We have used the NBT-II bladder carcinoma cell line as a model system to study the mechanisms of these events. Upon exposure to acidic fibroblast growth factor (aFGF), NBT-II cells undergo morphological changes that resemble those described in epithelial-mesenchymal transitions, i.e., dissociation of some or all polygonal epithelial cells and their transformation into motile, fibroblastic-like cells. The disruption of intercellular contacts, which accompanies cell dissociation and acquisition of motility, is correlated with a redistribution of E-cadherin, a Ca(2+)-dependent cell adhesion molecule, over the entire cell surface and within the cytoplasm. However, these modifications are not accompanied by a reduction of the intercellular adhesiveness or a loss of E-cadherin expression. Moreover, the formation of intercellular contacts between fibroblastic-like NBT-II cells results in the relocation of epithelial cadherin (E-cadherin) immunoreactivity on lateral membranes, but is not sufficient to abrogate cell motility. Finally, the overexpression of E-cadherin by NBT-II cells stably transfected with a plasmid containing the mouse E-cadherin cDNA does not impair the scattering effect of aFGF, indicating that high levels of E-cadherin expression do not prevent cells from disrupting their intercellular connections. Altogether, these results suggest that the scattering activity of aFGF is not mediated by direct modulations of E-cadherin expression.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Cadherins / metabolism*
  • Cell Adhesion
  • Cell Movement
  • Cytoplasm / metabolism
  • Cytoskeletal Proteins / metabolism*
  • Fibroblast Growth Factor 1 / pharmacology*
  • Genetic Vectors
  • Intercellular Junctions / metabolism
  • Phosphorylation
  • Rats
  • Tumor Cells, Cultured / drug effects*


  • Cadherins
  • Cytoskeletal Proteins
  • Fibroblast Growth Factor 1