Journal
NEUROCHEMICAL RESEARCH
Volume 42, Issue 3, Pages 918-924Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-016-2044-4
Keywords
Glioblastoma; AKT; GSK3 beta; Therapeutic target
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Funding
- National Scientific Leading Centre (KNOW-MMRC)
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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 beta (GSK3 beta), a target of AKT. In this review we focus on the function of AKT/GSK3 beta signaling in GBM.
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