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      Modulation of hepatocyte growth factor-induced scattering of HT29 colon carcinoma cells. Involvement of the MAPK pathway.

      Journal of Cell Science
      Actins, analysis, Arachidonic Acid, pharmacology, Calcium-Calmodulin-Dependent Protein Kinases, antagonists & inhibitors, metabolism, Carcinogens, Cell Adhesion, drug effects, physiology, Cell Movement, Collagen, Desmosomes, chemistry, Enzyme Inhibitors, Extracellular Matrix Proteins, Flavonoids, HT29 Cells, cytology, enzymology, Hepatocyte Growth Factor, Humans, Laminin, Signal Transduction, Tetradecanoylphorbol Acetate

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          Abstract

          Hepatocyte growth factor (HGF)/scatter factor modulates the motility of HT29 colon carcinoma cells in vitro by inducing morphological changes that depend on the type of extra-cellular matrix (ECM) ligand; HGF-induced scattering of HT29 cells is observed if cells are grown on plastic coated with serum proteins but not laminin. The absence of scattering correlates with a lack of cell spreading on laminin and it is not due to impaired HGF induced tyrosine phosphorylation of the E-cadherin/desmosome component, (gamma)-catenin, or lack of activation of mitogen activated protein kinase (MAPK). Treatment of HT29 cells with phorbol 12-myristate, 13-acetate (PMA), but not arachidonic acid, restored the ability of the cells to spread on laminin in an integrin-dependent manner. Moreover, the addition of both PMA and HGF restored the ability of these cells to scatter on laminin in a synergistic manner. This event correlated with increased tyrosine phosphorylation of paxillin and activation of MAPK. Moreover, when the MEK (MAPK kinase)/MAPK pathway was blocked by the MEK inhibitor PD098059, HGF-induced scattering of HT29 cells was blocked. Thus, HGF modulation of HT29 cell motility is regulated by both integrin and growth factor-dependent signaling and implicates MAPK in the modulation of intercellular adhesion and epithelial cell motility.

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