Propofol mediates non‐small cell lung cancer growth in part by regulating circ_0003028‐related mechanisms

BACKGROUND: Circular RNAs (circRNAs) are associated with propofol‐mediated inhibitory effect on non‐small cell lung cancer (NSCLC) progression. Circular hsa_circ_0003028 (circ_0003028) exerts a tumor‐promoting role in NSCLC. However, it is unclear whether propofol can mediate NSCLC progression via regulating circ_0003028 expression. METHODS: A total of 36 NSCLC patients were recruited in the study. Cell viability, proliferation, apoptosis, migration, and invasion were determined by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT), colony formation, flow cytometry, and transwell assays. Relative expression of circ_0003028 in NSCLC samples and cells was detected by quantitative real‐time polymerase chain reaction (RT‐qPCR). Analysis of the latent binding of circ_0003028 to miR‐1305 was done by bioinformatic analysis and confirmed by luciferase reporter and RNA immunoprecipitation (RIP) assays. Xenografting in mice was done to verify the relationship between propofol and circ_0003028. RESULTS: Significant upregulation of circ_0003028 was detected in NSCLC samples and cells. Functionally, propofol treatment reduced circ_0003028 expression in NSCLC cells, and circ_0003028 overexpression impaired propofol‐mediated inhibitory effect on NSCLC cell proliferation, migration, and invasion. Interestingly, circ_0003028 could compete with miR‐1305 as a competing endogenous RNA and upregulate CORO1C expression in NSCLC cells. CONCLUSION: Propofol‐mediated inhibiting effect on NSCLC growth partly depended on the circ_0003028/miR‐1305/CORO1C axis.