DANCR promotes glioma cell autophagy and proliferation via the miR-33b/DLX6/ATG7 axis

Long non-coding RNAs (lncRNAs) are common in the human body. Misregulated lncRNA expression can cause a variety of diseases in the human body. The present study aimed to investigate the effect of lncRNA differentiation antagonizing non-protein-coding RNA (DANCR) on glioma proliferation and autophagy through the microRNA (miR)-33b/distal-less homeobox 6 (DLX6)/autophagy-related 7 (ATG7) axis. Reverse transcription-quantitative PCR was used to detect DANCR and miR-33b expression. Cell Counting Kit-8 assay and flow cytometry were used to detect cell proliferation and apoptosis, respectively. Transmission electron microscopy was used to determine the autophagy level by observing intracellular autophagosomes. A western blot assay was used to detect protein expression levels and determine the level of autophagy in different cells. The binding sites of miR-33b and DANCR or DLX6 were detected using a dual-luciferase reporter assay. A chromatin immunoprecipitation assay confirmed DLX6 as a transcript of ATG7. In vivo tumorigenesis of glioma cells was validated in nude mice. DANCR and DLX6 were highly expressed in glioma cells, while miR-33b showed low expression in glioma cells. DANCR reduced the targeted binding of miR-33b to DLX6 by sponging miR-33b. The result verified that DANCR could promote ATG7 protein expression through miR-33b/DLX6, promote intracellular autophagy and proliferation and reduce apoptosis. The present study identified the role of the DANCR/miR-33b/DLX6/ATG7 axis in regulating autophagy, proliferation, and apoptosis in glioma cells, providing new ideas for glioma treatment.