SP1 诱导的长链非编码 RNA CASC11 通过海绵吸附 miR-498 靶向 FOXK1 加速脑胶质瘤发生。
SP1 induced lncRNA CASC11 accelerates the glioma tumorigenesis through targeting FOXK1 via sponging miR-498.
机构信息
Department of Neurosurgery, The First Affiliated Hospital of Xi 'an Jiaotong University, Xi'an, 710061, PR China.
Department of Neurosurgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, 710038, PR China.
出版信息
Biomed Pharmacother. 2019 Aug;116:108968. doi: 10.1016/j.biopha.2019.108968. Epub 2019 May 20.
The biological functions of long noncoding RNAs (lncRNAs) in the glioma have gained much attention in recent researches. However, the deepgoing mechanism by which lncRNA regulates the gliomagenesis is still ambiguous. In this work, we found that lncRNA CASC11 was significantly up-regulated in the glioma specimens and cells, and the ectopic overexpression indicated the poor prognosis of glioma patients. CASC11 expression could be activated by the transcription factor SP1. In vivo and vitro, the knockdown of CASC11 impaired the proliferation, migration and tumor growth of glioma cells. In mechanical experiments, the miR-498 was found to target the 3'-UTR of lncRNA CASC11 and FOXK1 mRNA. Taken together, the data suggest the regulation of SP1/CASC11/miR-498/FOXK1 in the gliomagenesis, which might provide a potential therapeutic strategy for glioma.
长链非编码 RNA（lncRNA）在神经胶质瘤中的生物学功能在最近的研究中受到了广泛关注。然而，lncRNA 调节神经胶质瘤发生的深入机制仍不清楚。在这项工作中，我们发现 lncRNA CASC11 在神经胶质瘤标本和细胞中显著上调，过表达表明神经胶质瘤患者的预后不良。CASC11 的表达可以被转录因子 SP1 激活。在体内和体外，CASC11 的敲低均会损害神经胶质瘤细胞的增殖、迁移和肿瘤生长。在机械实验中，发现 miR-498 靶向 lncRNA CASC11 和 FOXK1 mRNA 的 3'-UTR。综上所述，数据表明 SP1/CASC11/miR-498/FOXK1 调节神经胶质瘤发生，这可能为神经胶质瘤提供一种潜在的治疗策略。
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