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.