Long non-coding RNAs (lncRNAs) have been reported to biologically regulate tumor progression. LncRNA MIR31HG has been identified as an oncogene in several cancer types, but its role and mechanism in glioblastoma (GBM) remain to be explored. In the present study, we detected strongly-expressed MIR31HG in GBM cells through RT-qPCR analysis. Through loss-of-function assays, we uncovered that MIR31HG exerted its oncogenic property in GBM through boosting cell proliferation and suppressing the apoptosis. Mechanistically, STAT1 was found to be as a transcription factor and played a part in activating the transcription of MIR31HG with upregulating the expression of MIR31HG in GBM. Moreover, high MIR31HG level was confirmed to induce the activation of Wnt/β-catenin signaling pathway in a variety of cancers. From subcellular fractionation and western blot assays, it was displayed that MIR31HG activated Wnt/β-catenin signaling pathway through enhancing the nuclear translocation of β-catenin. Rescue assays showed that the treatment of LiCl countervailed MIR31HG depletion-induced inhibition on GBM cell growth. In conclusion, STAT1-induced upregulation of lncRNA MIR31HG facilitates GBM cell growth by activating Wnt/β-catenin signaling pathway.

据报道，长非编码 RNA (lncRNA) 可从生物学角度调节肿瘤进展。 LncRNA MIR31HG 已被确定为多种癌症类型的癌基因，但其在胶质母细胞瘤 (GBM) 中的作用和机制仍有待探索。在本研究中，我们通过 RT-qPCR 分析检测到 GBM 细胞中强表达的 MIR31HG。通过功能丧失检测，我们发现 MIR31HG 通过促进细胞增殖和抑制细胞凋亡在 GBM 中发挥其致癌特性。从机制上讲，STAT1被发现是一种转录因子，参与激活MIR31HG的转录，上调GBM中MIR31HG的表达。此外，高MIR31HG水平被证实可诱导多种癌症中Wnt/β-catenin信号通路的激活。亚细胞分级分离和蛋白质印迹实验表明，MIR31HG 通过增强 β-catenin 的核转位来激活 Wnt/β-catenin 信号通路。救援试验表明，LiCl 处理可以抵消 MIR31HG 耗竭引起的 GBM 细胞生长抑制。总之，STAT1诱导的lncRNA MIR31HG上调通过激活Wnt/β-catenin信号通路促进GBM细胞生长。