Background: Glioma is a malignant brain tumor with poor prognosis. Sevoflurane has been shown to have antitumor effects in various cancers. However, the underlying role and mechanism of sevoflurane in glioma is still unclear. Materials and Methods: Glioma cell lines were exposed different concentrations of sevoflurane (sev). The cell proliferation and migration were examined by Cell Counting Kit-8 (CCK-8) and Transwell assays, respectively. All protein levels were measured by Western blot. The levels of noncoding RNA in the INK4 locus (ANRIL) and let-7b-5p were detected by quantitative real-time polymerase chain reaction. The binding sites between ANRIL and let-7b-5p were predicted by StarBase v.3.0 and confirmed using dual-luciferase reporter assay. Results: Sevoflurane treatment suppressed proliferation and migration of glioma cells. The expression of ANRIL was downregulated in glioma cells after treatment with sevoflurane in a dose-dependent manner, and overexpression of ANRIL reversed sevoflurane-induced inhibition of proliferation and migration of glioma cells. Furthermore, let-7b-5p was targeted by ANRIL, and ANRIL knockdown recovered the promoting effects of silencing let-7b-5p on proliferation, migration, and JAK2/STAT3 pathway in sevoflurane-treated glioma cells. Conclusions: Sevoflurane hindered proliferation and migration through JAK2/STAT3 pathway mediated by ANRIL and let-7b-5p in glioma cells, indicating a new reference for the application of anesthetics like sevoflurane in glioma.
Keywords: ANRIL; glioma; let-7b-5p; progression; sevoflurane.