Sevoflurane represses the progression of glioma by the regulation of circ_0037655/miR-130a-5p/RPN2 axis.

Sevoflurane (SEV) is a common anesthetic to inhibit glioma progression. The previous studies have indicated the molecular mechanisms of SEV function in glioma. The objective of this study was to explore the association of circ_00037655 with SEV in glioma. Cell viability was evaluated by Cell Counting Kit-8 (CCK-8) assay. Cell proliferation was analyzed using Edu assay and colony formation assay. Flow cytometry was applied to determine cell apoptosis. Protein analysis was performed via western blot. Cell migration and invasion were assessed by transwell assay. Circ_0037655, microRNA-130a-5p (miR-130a-5p) and ribophorin II (RPN2) levels were detected using the quantitative real-time polymerase chain reaction (qRT-PCR). Dual-luciferase reporter, RNA immunoprecipitation (RIP) and pull-down assays were used to analyze target interaction. The effect of circ_0037655 on SEV in vivo was researched by xenograft models. SEV reduced cell viability, proliferation, migration and invasion but induced apoptosis of glioma cells. Circ_0037655 expression was inhibited after SEV treatment in glioma cells. The effects of SEV on glioma cell behaviors were attenuated by upregulation of circ_0037655. Circ_0037655 interacted with miR-130a-5p and miR-130a-5p targeted RPN2. Circ_0037655 or miR-130a-5p regulated the anti-tumor function of SEV in glioma by targeting miR-130a-5p or RPN2. Circ_0037655 affected the expression of RPN2 via targeting miR-130a-5p. Circ_0037655 relieved SEV-induced glioma growth inhibition in vivo by mediating miR-130a-5p and RPN2 levels. SEV inhibited the malignant progression of glioma cells partly by regulating the circ_0037655/miR-130a-5p/RPN2 axis.