Abstract: Objective To investigate the effect of propofol on invasion and migration of esophageal squamous cancer cell line KYSE150 and potential mechanism. Methods KYSE150 cells were treated with 0, 2.5, 5 and 10 μg/L propofol,Transwell chamber and scratch assay were used to detect the invasion and migration of cells after 24 h. RT-qPCR was used to detect the expression of miR-218 in cells. Western blot analysis was performed to detect the expression of HMGB1 protein. Bioinformatics software prediction and dual luciferase reporter gene assay were performed to detect the targeting relationship between miR-218 and HMGB1, Western blot to detect the regulation of miR-218 on HMGB1 protein. After transfection of miR-218 inhibitor or pcDNA3.1-HMGB1-GFP over-expression vector plasmid was constructed by liposome method, the expression of miR-218 was detected by RT-qPCR, the expression of HMGB1 protein was detected by Western blot, Transwell chamber and scratch test. The effect of down-regulating miR-218 or up-regulating HMGB1 expression on invasion and migration of 10 μg/L propofol-treated KYSE150 cells was examined. Results Propofol inhibited the invasion, migration and expression of HMGB1 protein in KYSE150 cells in a concentration-dependent manner and promoted the expression of miR-218. Dual luciferase reporter gene experiments confirmed that HMGB1 was a target gene of miR-218, and Western blot analysis confirmed that miR-218 negatively regulated the expression of HMGB1 protein. Down-regulation of miR-218 expression reversed the inhibitory effect of propofol on invasion and migration of KYSE150 cells. Up-regulation of HMGB1 expression reversed the inhibitory effect of propofol on invasion and migration of KYSE150 cells. Conclusions miR-218 plays an active role in the inhibition of invasion and migration of esophageal squamous cell carcinoma KYSE150 cells by propofol, and its mechanism is potentially related to targeted regulation of HMGB1.

Key words: propofol, miR-218, invasion, migration, HMGB1