Bex2 regulates cell proliferation and apoptosis in malignant glioma cells via the c-Jun NH2-terminal kinase pathway

Biochem Biophys Res Commun. 2012 Oct 26;427(3):574-80. doi: 10.1016/j.bbrc.2012.09.100. Epub 2012 Sep 26.

Abstract

The function of Bex2, a member of the Brain Expressed X-linked gene family, in glioma is controversial and its mechanism is largely unknown. We report here that Bex2 regulates cell proliferation and apoptosis in malignant glioma cells via the c-Jun NH2-terminal kinase (JNK) pathway. The expression level of Bex2 is markedly increased in glioma tissues. We observed that Bex2 over-expression promotes cell proliferation, while down-regulation of Bex2 inhibits cell growth. Furthermore, Bex2 down-regulation promotes cell apoptosis and activates the JNK pathway; these effects were abolished by administration of the JNK specific inhibitor, SP600125. Thus, Bex2 may be an important player during the development of glioma.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anthracenes / pharmacology
  • Apoptosis*
  • Cell Line, Tumor
  • Cell Proliferation*
  • Down-Regulation
  • Glioma / metabolism
  • Glioma / pathology*
  • Humans
  • JNK Mitogen-Activated Protein Kinases / antagonists & inhibitors
  • JNK Mitogen-Activated Protein Kinases / metabolism*
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / metabolism*
  • Protein Kinase Inhibitors / pharmacology
  • Signal Transduction

Substances

  • Anthracenes
  • BEX2 protein, human
  • Nerve Tissue Proteins
  • Protein Kinase Inhibitors
  • pyrazolanthrone
  • JNK Mitogen-Activated Protein Kinases