Sevoflurane suppresses glioma tumorigenesis via regulating circ_0079593/ miR-633/ROCK1 axis

Background: Sevoflurane is a common inhalational anesthetic, which has been revealed to have anticancer effect in glioma. However, the mechanisms of sevoflurane in glioma progression remain largely unclear. Methods: Cell proliferation, cell cycle, apoptosis and metastasis were monitored by cell counting kit-8 (CCK-8), flow cytometry, Transwell and Western blot assays. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot assays were used to examine the expression levels of circ_0079593, microRNA (miR)-633 and ROCK1 (Rho Associated Coiled-Coil Containing Protein Kinase 1). The dual-luciferase reporter assay was employed to confirm the targeting relationship between miR-633 and circ_0079593 or ROCK1. Animal experiment was conducted to explore the effect of sevoflurane in vivo. Results: Sevoflurane inhibited glioma cell proliferation, metastasis and induced apoptosis in vitro as well as impeded tumor growth in vivo. The expression of circ_0079593 was higher in glioma tissues and cells, and was decreased by sevoflurane treatment in glioma cells. Functional experiments showed that circ_0079593 overexpression in glioma cells reversed the inhibitory effects of sevoflurane on cell growth and metastasis. In a mechanism analysis, circ_0079593 acted as a sponge for miR-633 to elevate ROCK1 expression in glioma cells, and sevoflurane could regulate ROCK1 expression via circ_0079593/miR-633 axis. Besides that, circ_0079593/ miR-633/ROCK1 axis mediated the protective effects of sevoflurane on glioma cell tumorigenesis. Conclusion: Sevoflurane repressed glioma tumorigenesis via regulating circ_0079593/miR-633/ROCK1 axis, suggesting a new insight into the application of sevoflurane in glioma therapy.

Automated summary

Sevoflurane inhibits glioma tumorigenesis by regulating the circ_0079593/miR-633/ROCK1 axis, providing a new perspective on the application of sevoflurane in glioma therapy.