Bim-dependent apoptosis follows IGFBP-5 down-regulation in neuroblastoma cells

Biochem Biophys Res Commun. 2006 Dec 15;351(2):547-52. doi: 10.1016/j.bbrc.2006.10.062. Epub 2006 Oct 18.

Abstract

The insulin-like growth factor (IGF) axis is frequently activated in neuroblastoma (NB) tumors and cell lines. We show that silencing endogenous expression of IGF Binding Protein-5 (IGFBP-5) in NB cells by using microRNA and siRNA causes mitochondrial apoptosis that is characterized by: (a) release of cytochrome C in the cytoplasm and activation of caspase 9; (b) Erk1 and Erk2 inhibition; and (c) upregulation of pro-apoptotic proteins Bim and Bax. Bim upregulation is caused, at least in part, by protein stabilization that may depend on inhibition of Erk1 and Erk2. Of interest, Bim knock-down by siRNA decreases apoptosis in IGFBP-5-interfered cells. Thus, inhibition of endogenously produced IGFBP-5 is associated with Bim-dependent apoptosis in NB cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis Regulatory Proteins / physiology*
  • Apoptosis*
  • Bcl-2-Like Protein 11
  • Cell Line, Tumor
  • Down-Regulation
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Humans
  • Insulin-Like Growth Factor Binding Protein 5 / biosynthesis*
  • Membrane Proteins / physiology*
  • Mitochondria / physiology
  • Neuroblastoma
  • Proto-Oncogene Proteins / physiology*
  • bcl-2-Associated X Protein / metabolism

Substances

  • Apoptosis Regulatory Proteins
  • BCL2L11 protein, human
  • Bcl-2-Like Protein 11
  • Insulin-Like Growth Factor Binding Protein 5
  • Membrane Proteins
  • Proto-Oncogene Proteins
  • bcl-2-Associated X Protein
  • Extracellular Signal-Regulated MAP Kinases