ETV2 mediates endothelial transdifferentiation of glioblastoma
作者机构：Department of MolecularCell and Developmental BiologyUniversity of California-Los AngelesLos AngelesCA 90095USA Blood Research LaboratoryChengdu Blood CenterSichuanChina State Key Laboratory of Biotherapy and Cancer CenterWest China HospitalSichuan Universityand Collaborative Innovation Center for BiotherapySichuanChina
出 版 物：《Signal Transduction and Targeted Therapy》 (信号转导与靶向治疗（英文）)
年 卷 期：2018年第3卷第1期
页 面：291-301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：This work was supported by grants from the National Natural Science Foundation of China(Grant no.81402275,81502522 and 81500153) Guangdong Innovative Research Team Program(Grand 2011Y073) China Postdoctoral Science Foundation(58-2549) CSCO-MERCK SERONO ONCOLOGY RESEARCH FUND(Y-MX2015-018)
摘 要：Glioblastoma multiforme(GBM)is characterized by extensive endothelial *** studies suggest that a subpopulation of endothelial cells originates via vasculogenesis by the transdifferentiation of GBM tumor cells into endothelial cells(endotransdifferentiation).The molecular mechanism underlying this process remains poorly ***,we show that the expression of ETS variant 2(ETV2),a master regulator of endothelial cell development,is highly correlated with *** studies demonstrate that ETV2 is sufficient and necessary for the transdifferentiation of a subpopulation of CD133+/Nestin+GBM/neural stem cells to an endothelial *** studies of ChIP-Seq with gain-of-function RNA-Seq data sets suggest that ETV2,in addition to activating vascular genes,represses proneural genes to direct *** endotransdifferentiation by ETV2 is VEGF-A independent,it likely accounts for the observed resistance of GBM tumor cells to antiangiogenesis *** characterization of the regulatory networks mediated by ETV2 in endo-transdifferentiation of GBM tumor cells should lead to the identification of more effective therapeutic targets for GBM.
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