AKT/GSK3β Signaling in Glioblastoma.
AKT/GSK3β Signaling in Glioblastoma.
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DOI：
10.1007/s11064-016-2044-4
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发表时间：
2017-03
影响因子：
4.4
通讯作者：
Szeliga M
中科院分区：
文献类型：
--
作者：
Majewska E;Szeliga M
胶质母细胞瘤（GBM）是最具侵袭性的原发性脑肿瘤。尽管在过去的十年中，对胶质瘤发病机制的生物学理解取得了进展，但GBM患者的临床结局仍然很差。参与生长、存活、迁移和对治疗的抗性的许多信号传导途径的失调已经涉及GBM的发病机制。这些途径之一是磷脂酰肌醇-3激酶（PI 3 K）/蛋白激酶B（AKT）/雷帕霉素敏感性mTOR复合物（mTOR）途径，迄今为止已被深入研究和广泛描述。AKT的作用靶点之一糖原合成酶激酶3 β（GSK 3 β）的作用却很少受到关注。本文就AKT/GSK 3 β信号通路在GBM中的作用作一综述。
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.