Long noncoding RNA DLX6-AS1 accelerates the glioma carcinogenesis by competing endogenous sponging miR-197-5p to relieve E2F1.

Long noncoding RNAs (lncRNAs) participate in numerous of human cancer tumorigenesis. Nevertheless, the in-depth molecular mechanism that lncRNAs regulate the gliomagenesis is still ambiguous. In this research, our study invests energy in the biologic roles of lncRNA DLX6-AS1 on the glioma tumorigenesis. Here, we demonstrated that DLX6-AS1 expression was both high-expressed in the glioma cells and tissue, and the overexpression of DLX6-AS1 was clinically correlated with the poor outcome of glioma patients. In the cellular functional assays, silenced DLX6-AS1 expression by siRNAs inhibited the proliferation, invasion and tumor growth in vitro and in vivo, while the enhanced DLX6-AS1 expression by plasmids promotes them. The bioinformatics predictive tools, luciferase reporter assay and correlation analysis found that miR-197-5p could both target the 3'-UTR of DLX6-AS1 as well as E2F1 gene, constructing DLX6-AS1-miR-197-5p-E2F1 axis. Moreover, receiver operating characteristic (ROC) curve analysis revealed that lncRNA DLX6-AS1 has valuable diagnostic value clinical diagnose for the glioma patients (AUC = 0.736). Overall, our finding supports that DLX6-AS1 accelerates the glioma carcinogenesis by competing endogenous sponging miR-197-5p to relieve E2F1, acting as a novel therapeutic target for glioma.