DANCR promotes glioma cell autophagy and proliferation via the miR‑33b/DLX6/ATG7 axis
Affiliations: Department of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China
- Published online on: January 4, 2023 https://doi.org/10.3892/or.2023.8476
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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.