Propofol Suppresses Glioma Tumorigenesis by Regulating circ_0047688/miR-516b-5p/IFI30 Axis

Propofol has recently attracted increasing attention for its anti-tumor property in cancers, including glioma. Circular RNAs (circRNAs) can act as key regulators in various cancers. However, the relationship between propofol and circ_0047688 in glioma is still unclear. Cell proliferation was evaluated by Cell Counting Kit-8 (CCK-8), 5-ethynyl-2 '-deoxyuridine (EdU), and colony formation assays. Cell migration and invasion were determined using transwell assay. Cell apoptosis was detected by flow cytometry. Protein levels and RNA levels were detected by western blot assay and real-time quantitative polymerase chain reaction (RT-qPCR), respectively. The intermolecular interaction was predicted by bioinformatics analysis and verified by dual-luciferase reporter assay. A mouse xenograft model was established for in vivo experiments. Propofol inhibited cell proliferation, migration, and invasion and accelerated apoptosis in glioma cells. Circ_0047688 was upregulated in glioma tissues and cells, and propofol downregulated circ_0047688 in a dose-dependent manner. Circ_0047688 knockdown inhibited glioma cell progression and its overexpression abated the anti-tumor role of propofol in glioma cells. Moreover, miR-516b-5p was a direct target of circ_0047688, and circ_0047688 promoted glioma cell progression by sponging miR-516b-5p. In addition, IFI30 was a direct target of miR-516b-5p, and miR-516b-5p inhibited glioma cell malignant behaviors by targeting IFI30 in propofol-treated cells. Furthermore, circ_0047688 overexpression could weaken the anti-tumor role of propofol in vivo. Propofol inhibited glioma progression via modulating circ_0047688/miR-516b-5p/IFI30 axis, providing a potential therapeutic strategy for treatment of glioma.