• Li Zhang, Hao Chen, Changzheng Tian, and Deli Zheng.
• Department of Anesthesiology, The First Hospital of Hebei Medicine University, Shijiazhuang, China.
• World Neurosurg. 2021 Sep 1; 153: e46-e58.

BackgroundGlioma is a common primary intracranial tumor, with high infiltration and aggression. Propofol (Pro) is associated with growth and metastasis in glioma. Meanwhile, circular RNA non-SMC condensin I complex subunit G (circNCAPG; hsa_circ_0007244) has been reported to be upregulated in glioma. This study explored the role and mechanism of circNCAPG in Pro-induced glioma progression.MethodsCell viability was determined by cell counting kit-8 assay. Levels of circNCAPG, microRNA-200a-3p (miR-200a-3p), and member RAS oncogene family (RAB5A) were detected by real-time quantitative polymerase chain reaction. Colony number, apoptosis, migration, and invasion were analyzed by colony formation, flow cytometry, wound healing, and transwell assays. Matrix metallopeptidase 2, matrix metallopeptidase 9, and RAB5A protein levels were detected by Western blot assay. The binding relationship between miR-200a-3p and circNCAPG or RAB5A was predicted by starBase 2.0 and then verified by a dual-luciferase reporter and RNA immunoprecipitation assays. The biological roles of circNCAPG and Pro on glioma tumor growth were examined by the xenograft tumor model in vivo.ResultsExpression of circNCAPG and RAB5A was upregulated, and miR-200a-3p was decreased in glioma tissues and cells, while their expression presented an opposite trend in Pro-treated glioma cells. Moreover, circNCAPG overexpression could abolish Pro-mediated proliferation, apoptosis, migration, and invasion in glioma cells in vitro. Mechanically, circNCAPG could regulate RAB5A expression by sponging miR-200a-3p. Pro blocked glioma tumor growth in vivo by modulating circNCAPG.ConclusionsPro could inhibit glioma cell growth and metastasis through the circNCAPG/miR-200a-3p/RAB5A axis, providing a promising therapeutic strategy for glioma treatment.Copyright © 2021. Published by Elsevier Inc.

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