Propofol Represses Cell Growth and Metastasis by Modulating the Circular RNA Non-SMC Condensin I Complex Subunit G/MicroRNA-200a-3p/RAB5A Axis in Glioma

-BACKGROUND: Glioma is a common primary intracran ial 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. -METHODS: Cell viability was determined by cell counting kit-8 assay. Levels of circNCAPG, microRNA-200a3p (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. -RESULTS: Expression of circNCAPG and RAB5A was u pregulated, 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. -CONCLUSIONS: Pro could inhibit glioma cell growth and metastasis through the circNCAPG/miR-200a-3p/RAB5A axis, providing a promising therapeutic strategy for glioma treatment.

Automated summary

This study discovered that circNCAPG and RAB5A were upregulated in glioma, while miR-200a-3p was decreased, with opposite trends in Pro-treated glioma cells. Overexpression of circNCAPG abolished Pro-mediated proliferation, apoptosis, migration, and invasion in glioma cells in vitro. Pro inhibited glioma tumor growth in vivo through modulation of circNCAPG.