Propofol suppresses non-small cell lung cancer tumorigenesis by regulation of circ-RHOT1/miR-326/FOXM1 axis

Abstract Background Lung cancer is a common malignant tumor around the world. Propofol has been found to play an anti-tumor role. Therefore, the purpose of this study is to clarify the role and underlying molecular mechanisms of Propofol in non-small cell lung cancer (NSCLC). Methods The real-time quantitative polymerase chain reaction (RT-qPCR) assay was conducted to measure the expression levels of circular_RHOT1 (circ-RHOT1), microRNA (miR)-326, and Forkhead Box M1 (FOXM1) in tissues and cells. The proliferation of cell was determined by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-2H-tetrazol-3-ium bromide (MTT) and colony forming assays. The flow cytometry assay was used to evaluate cell apoptosis. The migration and invasion of NSCLC cells were determined by transwell assay. The protein expression level of FOXM1 was quantified by western blot assay. The association between miR-326 and circ-RHOT1 or FOXM1 was confirmed by dual-luciferase reporter assay. Results Circ-RHOT1 was increased in NSCLC tissues and cells. Importantly, treatment with Propofol inhibited circ-RHOT1 expression in NSCLC cells. Propofol dose-dependently inhibited proliferation, migration and invasion while induced apoptosis of NSCLC cells, which was abolished by circ-RHOT1 overexpression, FOXM1 overexpression, or miR-326 silencing. MiR-326, interacted with FOXM1, was a target of circ-RHOT1 in NSCLC cells, which was confirmed by dual-luciferase reporter assay. Circ-RHOT1 regulated FOXM1 expression by sponging miR-326 in NSCLC cells. In addition, inhibition of circ-RHOT1 in combined with Propofol impeded tumorigenesis in vivo. Conclusion Propofol repressed proliferation, migration and invasion while induced apoptosis of NSCLC cells at least in part by regulation of circ-RHOT1/miR-326/FOXM1 axis in NSCLC cells.