LncRNA MIR31HG is activated by STAT1 and facilitates glioblastoma cell growth via Wnt/β-catenin signaling pathway.

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.