Glycogen synthase kinase-3β (GSK-3β) and its dysregulation in glioblastoma multiforme

J Clin Neurosci. 2013 Sep;20(9):1185-92. doi: 10.1016/j.jocn.2013.02.003. Epub 2013 Jun 12.

Abstract

Glioblastoma multiforme (GBM) is the most frequently occurring and devastating human brain malignancy, retaining almost universal mortality and a median survival of only 14 months, even with recent advances in multimodal treatments. Gliomas are characterised as being both highly resistant to chemo- and radiotherapy and highly invasive, rendering conventional interventions palliative. The continual dismal prognosis for GBM patients identifies an urgent need for the evolutionary development of new treatment modalities. This includes molecular targeted therapies as many signaling molecules and associated pathways have been implicated in the development and survival of malignant gliomas including the protein kinase, glycogen synthase kinase 3 beta (GSK-3β). Here we review the activity and function of GSK-3β in a number of signaling pathways and its role in gliomagenesis.

Keywords: Cancer; GSK-3β; Glioblastoma multiforme; PI3-K; Wnt.

Publication types

  • Review

MeSH terms

  • Animals
  • Brain Neoplasms / enzymology*
  • Brain Neoplasms / pathology
  • Carcinogenesis / metabolism
  • Carcinogenesis / pathology
  • Glioblastoma / enzymology*
  • Glioblastoma / pathology
  • Glycogen Synthase Kinase 3 / chemistry
  • Glycogen Synthase Kinase 3 / physiology*
  • Glycogen Synthase Kinase 3 beta
  • Humans
  • Protein Binding / physiology
  • Protein Structure, Secondary
  • Signal Transduction / physiology

Substances

  • GSK3B protein, human
  • Glycogen Synthase Kinase 3 beta
  • Glycogen Synthase Kinase 3