Protein kinase C modulates negatively the hepatocyte growth factor-induced migration, integrin expression and phosphatidylinositol 3-kinase activation

Annamária Gujdár, Szabolcs Sipeki, Erzsébet Bander, László Buday, Anna Faragó

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Previously, we reported that, in hepatocyte growth factor (HGF)-induced HepG2 cells, protein kinase C (PKC) decreased the duration of intensive Erk1/Erk2 MAP kinase activation. This study shows that the inhibition of PKC enhanced significantly the HGF-induced integrin expression. Beside the prolonged activation of Erk1/Erk2, the activity of phosphatidylinositol 3-kinase (PI 3K) was required for growth factor-induced integrin expression. PI 3-kinase was activated to a higher extent in response to HGF than to epidermal growth factor (EGF), though the activation was transient in both cases. In EGF-induced cells, PI 3K activation was terminated by the loss of phosphotyrosine docking sites for PI 3K. To the contrary, the decrease of PI 3K activation, which followed the HGF-induced increase was not accompanied by the loss of phosphotyrosine docking sites and was prevented by the inhibition of PKC. The negative modulator effects of PKC on integrin expression and PI 3-kinase activation correlated with its ability to limit the HGF-induced motogen response.

Original languageEnglish
Pages (from-to)505-513
Number of pages9
JournalCellular Signalling
Volume16
Issue number4
DOIs
Publication statusPublished - Apr 2004

Keywords

  • Erk1/Erk2 MAP kinases
  • Gab1
  • HepG2 cells
  • Invasive growth
  • c-Met

ASJC Scopus subject areas

  • Cell Biology

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