ETV2 mediates endothelial transdifferentiation of glioblastoma

• DOI: 10.1038/s41392-018-0007-8
• Publication Date: 2018-02-07T11:56:56Z
• Authors: Chengjian Zhao; Gustavo A. Gomez; Yuwei Zhao; Yu Yang; Dan Cao; Jing Lu; Hanshuo Yang; Shuo Lin
• Keywords: Transdifferentiation

Glioblastoma multiforme (GBM) is characterized by extensive endothelial hyperplasia. Recent studies suggest that a subpopulation of cells originates via vasculogenesis the transdifferentiation GBM tumor into (endo-transdifferentiation). The molecular mechanism underlying this process remains poorly defined. Here, we show expression ETS variant 2 (ETV2), master regulator cell development, highly correlated with malignancy. Functional demonstrate ETV2 sufficient and necessary for CD133+/Nestin+ GBM/neural stem to an lineage. Combinational ChIP-Seq gain-of-function RNA-Seq data sets ETV2, in addition activating vascular genes, represses proneural genes direct endo-transdifferentiation. Since endo-transdifferentiation VEGF-A independent, it likely accounts observed resistance anti-angiogenesis therapy. Further characterization regulatory networks mediated should lead identification more effective therapeutic targets GBM.