The death receptor CD95 activates the cofilin pathway to stimulate tumour cell invasion

EMBO Rep. 2011 Sep 1;12(9):931-7. doi: 10.1038/embor.2011.129.

Abstract

The death receptor CD95 promotes apoptosis through well-defined signalling pathways. In colorectal cancer cells, CD95 primarily stimulates migration and invasion through pathways that are incompletely understood. Here, we identify a new CD95-activated tyrosine kinase pathway that is essential for CD95-stimulated tumour cell invasion. We show that CD95 promotes Tyr 783 phosphorylation of phospholipase C-γ1 through the platelet-derived growth factor receptor-β, resulting in ligand-stimulated phosphatidylinositol (4,5)-bisphosphate (PIP(2)) hydrolysis. PIP(2) hydrolysis liberates the actin-severing protein cofilin from the plasma membrane to initiate cortical actin remodelling. Cofilin activation is required for CD95-stimulated formation of membrane protrusions and increased tumour cell invasion.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actin Depolymerizing Factors / metabolism*
  • Actins / metabolism
  • Animals
  • Apoptosis
  • Cell Line, Tumor
  • Cell Membrane / metabolism
  • Cell Surface Extensions
  • Colorectal Neoplasms / metabolism*
  • Colorectal Neoplasms / pathology
  • Mice
  • Neoplasm Invasiveness
  • Phosphatidylinositols / metabolism*
  • Phospholipase C gamma / metabolism
  • Phosphorylation
  • Receptor, Platelet-Derived Growth Factor beta / metabolism
  • Receptors, Death Domain / metabolism
  • Signal Transduction*
  • fas Receptor / metabolism*

Substances

  • Actin Depolymerizing Factors
  • Actins
  • Phosphatidylinositols
  • Receptors, Death Domain
  • fas Receptor
  • Receptor, Platelet-Derived Growth Factor beta
  • Phospholipase C gamma