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.