sevoflurane regulates glioma progression by circ_0002755/mir-628-5p/magt1 axis

Haoyi Li,1,* Tian Xia,1,* Yilin Guan,2 Yao Yu1 1Department of Anaesthesiology, The Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116027, People’s Republic of China; 2Department of Anaesthesiology, Dalian Municipal Women and Children’s Medical Center, Dalian, Liaoning 116037, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yao YuDepartment of Anaesthesiology, The Second Affiliated Hospital of Dalian Medical University, NO. 467 Zhongshan Road, Dalian, Liaoning 116027, People’s Republic of ChinaTel +86 411-84671291Email summer930318@163.comBackground: Glioma is a common malignant tumor worldwide. Sevoflurane (Sev) has been reported to inhibit the metastasis of glioma cells, but the underlying molecular mechanism needs further exploration.Methods: Cell Counting Kit-8 (CCK8) assay was used to check cell viability. Flow cytometry assay was hired to check cell apoptosis. The protein levels of B-cell lymphoma-2 (Bcl-2), BCL2-Associated X (Bax), hexokinase 2 (HK2) and magnesium transporter 1 (MAGT1) in samples were measured by Western blot. The abilities of cell migration and invasion were estimated by transwell assay. Glucose colorimetric assay kit and lactate colorimetric assay kit were used to check glucose consumption and lactate production, respectively. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the levels of circular RNA (circRNA) circ_0002755 (also known as the circRNA1656) and microRNA (miR)-628-5p in samples. The interaction between miR-628-5p and circ_0002755 or MAGT1 was predicated by starBase, which was verified by the dual-luciferase reporter assay. Xenograft tumor model was established to explore the biological role of circ_0002755 in vivo.Results: Sev inhibited cell viability, migration, invasion and promoted cell apoptosis, and also reduced glucose consumption and lactate production. Circ_0002755 was significantly upregulated in glioma tissues and cells, while its level was notably declined under Sev treatment. Besides, overexpression of circ_0002755 overturned Sev-mediated inhibitory effect on glioma progression. Further research indicated that circ_0002755 targeted miR-628-5p, and miR-628-5p targeted MAGT1, and Sev modulated glioma progression via circ_0002755/miR-628-5p/MAGT1 axis. Moreover, Sev hindered tumor growth in vivo.Conclusion: Sev mediated glioma progression via circ_0002755/miR-628-5p/MAGT1 axis.Keywords: Sev, glioma, circ_0002755, miR-628-5p, MAGT1