Emerging function of mTORC2 as a core regulator in glioblastoma: metabolic reprogramming and drug resistance

作     者：Si-Han Wu Jun-Feng Bi Timothy Cloughesy Webster K.Cavenee Paul S.Mischel 

作者机构：Ludwig Institute for Cancer Research University of California Neuro-Oncology ProgramUniversity of California 

出 版 物：《Cancer Biology & Medicine》 (癌症生物学与医学（英文版）)

年 卷 期：2014年第11卷第4期

页      面：255-263页

核心收录：

学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

基　　金：supported by grants from the National Institute for Neurological Diseases and Stroke(NS73831) the National Cancer Institute(CA151819) The Ben and Catherine Ivy Foundation,the Defeat GBM Research Collaborative,a subsidiary of National Brain Tumor Society by the generous donations from the Ziering Family Foundation in memory of Sigi Ziering 

主　　题：Glioblastoma mTOR metabolic reprogramming mTORC2 Warburg effect PI3K 

摘      要：Glioblastoma （GBM） is one of the most lethal human cancers. Genomic analyses define the molecular architecture of GBM and highlight a central function for mechanistic target of rapamycin （roTOR） signaling, roTOR kinase exists in two multi- protein complexes, namely, mTORC 1 and mTORC2. These complexes differ in terms of function, regulation and rapamycin sensitivity, mTORC 1 is well established as a cancer drug target, whereas the functions of mTORC2 in cancer, including GBM, remains poorly understood. This study reviews the recent findings that demonstrate a central function ofmTORC2 in regulating tumor growth, metabolic reprogramming, and targeted therapy resistance in GBM, which makes mTORCZ as a critical GBM drug target.