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DDX3X促进ILF3的稳定性,通过M2巨细胞极化加速神经母细胞瘤的进展

Tian Lin¹, Xinghe Chen¹, He Huang¹

¹Department of Pediatric Surgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou 350005, China; Department of Pediatric Surgery, National Regional Medical Center, Binhai Campus of the First Affiliated Hospital, Fujian Medical University, Fuzhou 350212, China.

|November 28, 2025

概括

死亡盒螺旋酶3X结合 (DDX3X) 稳定了互白素增强剂结合因子3 (ILF3) mRNA,促进了神经母细胞瘤的进展和M2巨细胞的两极分化. 抑制DDX3X抑制了瘤生长和转移.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

神经母细胞瘤 (NB) 是一种预后不佳的儿科癌症.
大细胞两极分化显著影响NB的进展.
对于RNA结合蛋白DDX3X和ILF3在NB巨细胞极化中的作用尚不清楚.

研究的目的:

调查DDX3X-ILF3轴在调节巨细胞极化和促进NB恶性瘤中的作用.
阐明DDX3X和ILF3相互作用背后的分子机制.

主要方法:

用RT-qPCR,西式涂抹和ELISA来分析基因和蛋白质表达和细胞因子分泌.
通过lentiviral介导的淘汰和过度表达被用来研究基因功能.
用Transwell共同培养和小鼠模型 (异种移植和转移) 来进行体外和体内评估.
RIP-qPCR和Actinomycin D治疗评估了RNA稳定性和蛋白质-RNA相互作用.

主要成果:

在NB细胞中,ILF3表达被上调.
抑制DDX3X或ILF3抑制了NB细胞的活力,增殖,入侵和迁移.
DDX3X knockdown 降低了 ILF3 的 mRNA 稳定性和蛋白质水平,促进了 M1 巨细胞的两极分化.
在体内,DDX3X抑制剂RK-33抑制了NB瘤的生长和转移,增强了M1极化.
过度ILF3表达逆转了DDX3X敲击/抑制的抑制作用.

结论:

DDX3X通过稳定ILF3mRNA来促进NB的进展,这推动了M2巨细胞的两极分化.
针对DDX3X-ILF3轴为神经母细胞瘤提供了一个潜在的治疗策略.

关键词:

死亡盒螺旋酶3与X结合.介质蛋白增强剂结合因子3 巨细胞的两极分化神经母细胞瘤的神经母细胞瘤

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