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Published on: January 9, 2019
AKT/GSK3β Signaling in Glioblastoma
Ewelina Majewska1, Monika Szeliga2
1Department of Neurotoxicology, Mossakowski Medical Research Centre, Polish Academy of Sciences, 5 Pawińskiego Str., 02-106, Warsaw, Poland.
Abstract:
Glioblastoma (GBM) is the most aggressive of primary brain tumors. Despite the progress in understanding the biology of the pathogenesis of glioma made during the past decade, the clinical outcome of patients with GBM remains still poor. Deregulation of many signaling pathways involved in growth, survival, migration and resistance to treatment has been implicated in pathogenesis of GBM. One of these pathways is phosphatidylinositol-3 kinases (PI3K)/protein kinase B (AKT)/rapamycin-sensitive mTOR-complex (mTOR) pathway, intensively studied and widely described so far. Much less attention has been paid to the role of glycogen synthase kinase 3 β (GSK3β), a target of AKT. In this review we focus on the function of AKT/GSK3β signaling in GBM.
Insights
Glioblastoma (GBM) is a deadly brain cancer. This review explores the AKT/GSK3β pathway
Area of Science:
- Neuro-oncology
- Molecular Biology
- Cancer Signaling Pathways
Background:
- Glioblastoma (GBM) is the most aggressive primary brain tumor, with poor patient outcomes despite advances in understanding its biology.
- Numerous signaling pathways, including PI3K/AKT/mTOR, are implicated in GBM pathogenesis, affecting tumor growth, survival, migration, and treatment resistance.
- While the PI3K/AKT/mTOR pathway is well-studied, the role of glycogen synthase kinase 3 beta (GSK3β), an AKT target, in GBM is less understood.
Purpose of the Study:
- To review the function of the AKT/GSK3β signaling pathway in Glioblastoma.
- To highlight the underappreciated role of GSK3β in GBM pathogenesis.
- To consolidate current knowledge on AKT/GSK3β signaling in the context of GBM.
Main Methods:
- Literature review of existing studies on GBM.
- Analysis of signaling pathways involved in GBM pathogenesis.
- Focus on the AKT/GSK3β axis and its implications.
Main Results:
- Deregulation of signaling pathways is a key factor in GBM.
- The PI3K/AKT/mTOR pathway plays a significant role in GBM.
- GSK3β, as a target of AKT, warrants further investigation in GBM.
Conclusions:
- The AKT/GSK3β signaling pathway is crucial in Glioblastoma.
- Further research into GSK3β's role could reveal new therapeutic targets for GBM.
- Understanding this pathway is vital for improving GBM patient outcomes.
