首页> 美国卫生研究院文献>Neuro-Oncology >NPV-LDE-225 (Erismodegib) inhibits epithelial mesenchymal transition and self-renewal of glioblastoma initiating cells by regulating miR-21 miR-128 and miR-200
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NPV-LDE-225 (Erismodegib) inhibits epithelial mesenchymal transition and self-renewal of glioblastoma initiating cells by regulating miR-21 miR-128 and miR-200

机译:NPV-LDE-225(Erismodegib)通过调节miR-21miR-128和miR-200抑制胶质母细胞瘤起始细胞的上皮间质转化和自我更新

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摘要

BackgroundGlioblastoma multiforme is the most common form of primary brain tumor, often characterized by poor survival. Glioblastoma initiating cells (GICs) regulate self-renewal, differentiation, and tumor initiation properties and are involved in tumor growth, recurrence, and resistance to conventional treatments. The sonic hedgehog (SHH) signaling pathway is essential for normal development and embryonic morphogenesis. The objectives of this study were to examine the molecular mechanisms by which GIC characteristics are regulated by NPV-LDE-225 (Smoothened inhibitor; (2,2′-[[dihydro-2-(4-pyridinyl)-1,3(2H,4H)-pyrimidinediyl]bis(methylene)]bis[N,N-dimethylbenzenamine).
机译:背景多形胶质母细胞瘤是原发性脑肿瘤的最常见形式,通常以生存期较差为特征。胶质母细胞瘤起始细胞(GIC)调节自我更新,分化和肿瘤起始特性,并参与肿瘤生长,复发和对常规治疗的耐药性。声刺猬(SHH)信号传导通路对于正常发育和胚胎形态发生至关重要。这项研究的目的是研究NPV-LDE-225(柔顺的抑制剂;(2,2'-[[二氢-2-(4-吡啶基)-1,3(2H) ,4H)-嘧啶二基]双(亚甲基)]双[N,N-二甲基苯胺)。

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