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MEF promotes stemness in the pathogenesis of gliomas

机译:MEF促进神经胶质瘤发病机制中的干性

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High-grade gliomas are aggressive and uniformly fatal tumors, composed of a heterogeneous population of cells that include many with stem-cell-like properties. The acquisition of stem-like traits might contribute to glioma initiation, growth, and recurrence. Here we investigated the role of the transcription factor myeloid Elf-1 like factor (MEF, also known as ELF4) in gliomas. We found that MEF is highly expressed in both human and mouse glioblastomas and its absence impairs gliomagenesis in a PDGF-driven glioma mouse model. We show that modulation of MEF levels in both mouse neural stem cells and human glioblastoma cells has a significant impact on neurosphere formation. Moreover, we identify Sox2 as a direct downstream target of MEF. Taken together, our studies implicate MEF as a previously unrecognized gatekeeper gene in gliomagenesis that promotes stem cell characteristics through Sox2 activation.
机译:高级神经胶质瘤是侵袭性且致命性一致的肿瘤,由异质细胞群体组成,其中包括许多具有干细胞样特性的细胞。茎样性状的获得可能促进神经胶质瘤的发生,生长和复发。在这里,我们研究了神经胶质瘤中转录因子髓样Elf-1样因子(MEF,也称为ELF4)的作用。我们发现,MEF在人和小鼠胶质母细胞瘤中都高度表达,而它的缺失会损害PDGF驱动的神经胶质瘤小鼠模型中的胶质瘤发生。我们表明,在小鼠神经干细胞和人类胶质母细胞瘤细胞中的MEF水平的调制对神经球形成有重大影响。此外,我们确定Sox2为MEF的直接下游目标。综上所述,我们的研究表明MEF是胶质瘤发生中以前未被认识的关守基因,该基因通过Sox2激活促进干细胞特性。

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    《Cell stem cell》 |2012年第6期|共9页
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  • 正文语种 eng
  • 中图分类 细胞生物学;
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