Long noncoding RNA (lncRNA) DUXAP10 has been shown to act as an oncogene in various tumors; however, its roles in glioma progression have never been established. Here, we show that DUXAP10 is overexpressed in glioma tissues and cells. Loss of function experiments reveal that DUXAP10 knockdown has little effects on glioma cell viability, but significantly reduces the stemness of glioma cells, which is characterized as the decrease of stemness marker expression, tumor sphere-forming ability, and ALDH activity. RNA immunoprecipitation and immunofluorescence assays indicate that DUXAP10 can directly interact with HuR protein and suppress the cytoplasm-nuclear translocation of HuR, which subsequently enhances Sox12 mRNA stability in cytoplasm and thus increases Sox12 expression. Further rescuing experiments show that the HuR/Sox12 axis is responsible for DUXAP10-mediated effects on glioma cell stemness.

中文翻译：

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长链非编码 RNA DUXAP10 通过招募 HuR 增强 Sox12 mRNA 稳定性来促进胶质瘤细胞的干性

长链非编码 RNA (lncRNA) DUXAP10 已被证明在各种肿瘤中充当癌基因；然而，它在胶质瘤进展中的作用从未确定。在这里，我们显示 DUXAP10 在胶质瘤组织和细胞中过度表达。功能丧失实验表明，DUXAP10 敲低对胶质瘤细胞活力影响不大，但显着降低了胶质瘤细胞的干性，其特点是干性标志物表达、肿瘤球形成能力和 ALDH 活性降低。RNA 免疫沉淀和免疫荧光测定表明 DUXAP10 可以直接与 HuR 蛋白相互作用并抑制 HuR 的细胞质 - 核易位，从而增强 Sox12 mRNA 在细胞质中的稳定性，从而增加 Sox12 的表达。