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Akt2 and Akt3 play a pivotal role in malignant gliomas

Hideo Mure1, Kazuhito Matsuzaki, Keiko T Kitazato

  • 1Department of Neurosurgery, Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15, Kuramoto-cho, Tokushima, Tokushima 770-8503, Japan. gaudi0529@ybb.ne.jp

Neuro-Oncology
|February 20, 2010
PubMed

Insights

Akt2 and Akt3 isoforms are crucial for malignant glioma cell survival. Targeting these Akt isoforms shows promise for treating gliomas, unlike Akt1 which has no significant effect.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • The Akt pathway, a key phosphatidylinositol 3-kinase effector, is frequently activated in cancers like glioblastoma.
  • The specific roles and expression patterns of Akt isoforms (Akt1, Akt2, Akt3) in malignant gliomas remain unclear.

Purpose of the Study:

  • To investigate the expression profiles of Akt1, Akt2, and Akt3 isoforms in human astrocytomas and glioblastomas.
  • To elucidate the functional significance of each Akt isoform in malignant glioma cell biology.

Main Methods:

  • Analysis of Akt isoform protein and mRNA expression in glioma tissues and non-neoplastic controls.
  • RNA interference-mediated knock-down and plasmid-based over-expression of Akt isoforms in glioma cell lines (U87MG, T98G, TGB).

Main Results:

  • Akt1 expression was consistent across glioma and normal tissues.
  • Akt2 levels increased with malignancy grade, while Akt3 levels decreased.
  • Knock-down of Akt2 or Akt3 induced apoptosis via caspase-dependent pathways, whereas Akt1 knock-down had no effect on cell growth or survival.
  • Over-expression of Akt2 or Akt3 led to down-regulation of the other isoform; Akt3 exhibited high kinase activity in U87MG cells.

Conclusions:

  • Akt2 and Akt3 play significant roles in maintaining the viability of human malignant glioma cells.
  • Targeting Akt2 and Akt3 presents a potential therapeutic strategy for glioma treatment.

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