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Critical role for the catalytic activity of phospholipase C-gamma1 in epidermal growth factor-induced cell migration.

Abstract
Phospholipase C-gamma1 (PLC-gamma1), a tyrosine kinase substrate, has been implicated in the pathway for the epidermal growth factor receptor (EGFR)-induced cell migration. However, the underlying mechanism by which PLC-gamma1 mediates EGFR-induced cell migration remains elusive. In the present study, we sought to determine whether the lipase activity of PLC-gamma1 is required for EGFR-induced cell migration. We found that overexpression of PLC-gamma1 in squamous cell carcinoma SCC4 cells markedly enhanced EGF-induced PLC-gamma1 activation, intracellular calcium rise, and cell migration. This enhancement was abolished by mutational inactivation of the catalytic domain of PLC-gamma1. Inhibition of the downstream signaling processes mediated by the activity of phospholipase C (PLC) using IP(3) receptor inhibitor or intracellular calcium chelator blocked EGF-induced cell migration. These data indicate that EGF-induced cell migration is mediated by the lipase domain of PLC-gamma1 and the subsequent IP(3) generation and intracellular calcium mobilization.
AuthorsZhongjian Xie, Jian Peng, Sally D Pennypacker, Ying Chen
JournalBiochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 399 Issue 3 Pg. 425-8 (Aug 27 2010) ISSN: 1090-2104 [Electronic] United States
PMID20674545 (Publication Type: Journal Article, Research Support, N.I.H., Extramural)
CopyrightCopyright 2010 Elsevier Inc. All rights reserved.
Chemical References
  • Inositol 1,4,5-Trisphosphate Receptors
  • Epidermal Growth Factor
  • EGFR protein, human
  • ErbB Receptors
  • Phospholipase C gamma
  • Calcium
Topics
  • Calcium (metabolism)
  • Catalysis
  • Cell Line, Tumor
  • Cell Movement
  • Epidermal Growth Factor (metabolism, pharmacology)
  • ErbB Receptors (metabolism)
  • Humans
  • Inositol 1,4,5-Trisphosphate Receptors (agonists, metabolism)
  • Neoplasm Invasiveness
  • Phospholipase C gamma (metabolism)

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