AKT/GSK3β Signaling in Glioblastoma

被引:95
|
作者
Majewska, Ewelina [1 ]
Szeliga, Monika [1 ]
机构
[1] Polish Acad Sci, Dept Neurotoxicol, Mossakowski Med Res Ctr, 5 Pawinskiego Str, PL-02106 Warsaw, Poland
关键词
Glioblastoma; AKT; GSK3; beta; Therapeutic target; GLYCOGEN-SYNTHASE KINASE-3; ENZASTAURIN PLUS TEMOZOLOMIDE; GROWTH-RELATED VARIATIONS; STEM-LIKE CELLS; PROTEIN-KINASE; GLIOMA-CELLS; C-MYC; RADIATION-THERAPY; PHASE-II; PATHWAY;
D O I
10.1007/s11064-016-2044-4
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:918 / 924
页数:7
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