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

查看全文 作　　者：Si-Han [1]Wu;Jun-Feng [1]Bi;Timothy [2]Cloughesy;Webster [1]K.Cavenee;Paul [1]S.Mischel 机构地区：[1]Ludwig Institute for Cancer Research, University of California;[2]Neuro-Oncology Program,University of California 出　　处：《Cancer Biology & Medicine》索引2014年第11卷第4期,共9页 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 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(m TOR) signaling. m TOR kinase exists in two multiprotein complexes, namely, m TORC1 and m TORC2. These complexes differ in terms of function, regulation and rapamycin sensitivity. m TORC1 is well established as a cancer drug target, whereas the functions of m TORC2 in cancer, including GBM, remains poorly understood. This study reviews the recent findings that demonstrate a central function of m TORC2 in regulating tumor growth, metabolic reprogramming, and targeted therapy resistance in GBM, which makes m TORC2 as a critical GBM drug target. 关 键 词：重新编程 耐药性 母细胞 代谢 胶质 稳压器 雷帕霉素 药物靶标