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Updated: Aug 11, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Sodium vanadate inhibits apoptosis in malignant glioma cells: a role for Akt/PKB

L S Chin1, S F Murray, D H Harter

  • 1Department of Neurosurgery and Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, MD, USA. Ichin@surgery1.umaryland.edu

Journal of Biomedical Science
|May 27, 1999
PubMed

Insights

Sodium vanadate activates key cell signaling pathways, protecting glioma cells from apoptosis. This protective effect is mediated by phosphoinositide 3-kinase (PI3K) and Akt/PKB, highlighting the balance between cell proliferation and death.

Area of Science:

  • Molecular Biology
  • Cell Signaling
  • Cancer Research

Background:

  • The dual signal hypothesis posits that a single signal can trigger both apoptosis (programmed cell death) and proliferation.
  • Mitogen-activated protein kinase (MAPK) kinases like ERK and JNK are implicated in apoptosis, while Akt/PKB (a PI3K-stimulated kinase) inhibits it.
  • Understanding these pathways is crucial for developing targeted cancer therapies, particularly in glioma.

Purpose of the Study:

  • To investigate the roles of ERK, JNK, and Akt/PKB in a glioma model of apoptosis.
  • To elucidate the mechanism by which sodium vanadate affects cell death and proliferation in T98G glioma cells.

Main Methods:

  • Treatment of T98G glioma cells with K252a (apoptosis inducer) and sodium vanadate (protein tyrosine phosphatase inhibitor).
  • Assessment of kinase activation (ERK, JNK, Akt/PKB) and proliferation.
  • Evaluation of vanadate's protective effect against K252a-induced apoptosis, with and without the PI3K inhibitor wortmannin.

Main Results:

  • Sodium vanadate activated ERK, JNK, and Akt/PKB in T98G cells without stimulating proliferation.
  • Vanadate conferred protection against K252a-induced apoptosis.
  • This protective effect was abolished by wortmannin, indicating a critical role for PI3K and Akt/PKB.

Conclusions:

  • The phosphoinositide 3-kinase (PI3K)/Akt/PKB pathway mediates the anti-apoptotic effect of sodium vanadate in glioma cells.
  • The balance between protein phosphorylation pathways is a key determinant of cell proliferation and cell death.
  • These findings offer insights into regulating cell fate in glioma and potentially other cancers.

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