Modulation of ERK1/2 activity is crucial for sphingosine-induced death of glioma C6 cells

Acta Biochim Pol. 2005;52(4):927-30. Epub 2005 Nov 21.

Abstract

In this study the contribution of the ERK1/2 pathway to sphingosine-induced death and morphological changes of the actin cytoskeleton in glioma C6 cells was investigated. Surprisingly, the level of ERK1/2 phosphorylation does not change after incubation of cells with sphingosine. Despite this, sphingosine induces rounding and detachment of cells without formation of apoptotic bodies. To shed light on this process, a specific inhibitor of ERK1/2 phosphorylation, U0126, was used. Cells incubated simultaneously with sphingosine and U0126 not only detached, but also exhibited formation of apoptotic-like blebs. These data suggest that during sphingosine-induced glioma C6 cell death apoptotic blebbing is dependent on ERK1/2 signalling and occurs only when ERK1/2 activity is decreased or abolished.

MeSH terms

  • Animals
  • Butadienes / pharmacology
  • Cell Death / drug effects*
  • Cell Line, Tumor
  • Enzyme Inhibitors / pharmacology
  • Extracellular Signal-Regulated MAP Kinases / drug effects
  • Extracellular Signal-Regulated MAP Kinases / metabolism*
  • Glioma
  • Mitogen-Activated Protein Kinase 3 / drug effects
  • Mitogen-Activated Protein Kinase 3 / metabolism*
  • Nitriles / pharmacology
  • Phosphorylation
  • Rats
  • Sphingosine / pharmacology*

Substances

  • Butadienes
  • Enzyme Inhibitors
  • Nitriles
  • U 0126
  • Extracellular Signal-Regulated MAP Kinases
  • Mitogen-Activated Protein Kinase 3
  • Sphingosine