Glycogen synthase kinase-3β (GSK-3β) and its dysregulation in glioblastoma multiforme

被引:32
作者
Atkins, R. J. [1 ]
Stylli, S. S. [1 ,2 ]
Luwor, R. B. [1 ]
Kaye, A. H. [1 ,2 ]
Hovens, C. M. [1 ,3 ]
机构
[1] Univ Melbourne, Royal Melbourne Hosp, Dept Surg, Parkville, Vic 3050, Australia
[2] Royal Melbourne Hosp, Dept Neurosurg, Parkville, Vic 3050, Australia
[3] Epworth, Australian Prostate Canc Res Ctr, Richmond, Vic, Australia
关键词
Cancer; Glioblastoma multiforme; GSK-3; beta; PI3-K; Wnt; CONFERS ENHANCED TUMORIGENICITY; BRAIN-TUMOR CONSORTIUM; DUAL-KINASE MECHANISM; WNT CORECEPTOR LRP6; LONG-TERM SURVIVAL; GLIOMA STEM-CELLS; BETA-CATENIN; MALIGNANT GLIOMA; GROWTH-FACTOR; NEURONAL POLARITY;
D O I
10.1016/j.jocn.2013.02.003
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Glioblastoma multiforme (GBM) is the most frequently occurring and devastating human brain malignancy, retaining almost universal mortality and a median survival of only 14 months, even with recent advances in multimodal treatments. Gliomas are characterised as being both highly resistant to chemo- and radiotherapy and highly invasive, rendering conventional interventions palliative. The continual dismal prognosis for GBM patients identifies an urgent need for the evolutionary development of new treatment modalities. This includes molecular targeted therapies as many signaling molecules and associated pathways have been implicated in the development and survival of malignant gliomas including the protein kinase, glycogen synthase kinase 3 beta (GSK-3 beta). Here we review the activity and function of GSK-3 beta in a number of signaling pathways and its role in gliomagenesis. (C) 2013 Elsevier Ltd. All rights reserved.
引用
收藏
页码:1185 / 1192
页数:8
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