TROY is a component of the Nogo receptor complex and plays the key role in neuronal survival, migration, and differentiation. Here, we show the up-regulation of TROY in human glioma tissues and cells. Inhibition of TROY expression slowed glioma development in vivo and in vitro. Raf kinase inhibitor (RKIP) was found to interact with TROY. The physical interaction of TROY/RKIP was confirmed via co-immunoprecipitation (co-IP) assays. Furthermore, we found that the TROY/RKIP interaction was enhanced by fetal bovine serum (FBS) exposure, and TROY knockdown also led to down-regulation of NF-κB. Finally, disruption of the TROY/RKIP interaction using the TAT-TROY (234-371 aa) protein reduced the glioma development in xenografted mice. This suggests the TROY/RKIP interaction is a potential target for therapy of gliomas.

中文翻译：

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TROY与RKIP相互作用以促进神经胶质瘤的发展。

TROY是Nogo受体复合物的组成部分，在神经元存活，迁移和分化中起关键作用。在这里，我们显示了人类神经胶质瘤组织和细胞中TROY的上调。TROY表达的抑制减慢了体内外的神经胶质瘤的发展。发现Raf激酶抑制剂（RKIP）与TROY相互作用。TROY / RKIP的物理相互作用已通过免疫共沉淀（co-IP）分析得以证实。此外，我们发现胎牛血清（FBS）暴露增强了TROY / RKIP相互作用，并且TROY敲低还导致NF-κB的下调。最后，使用TAT-TROY（234-371 aa）蛋白破坏TROY / RKIP相互作用减少了异种移植小鼠的神经胶质瘤发展。这表明TROY / RKIP相互作用是神经胶质瘤治疗的潜在目标。