Sevoflurane inhibits the migration, invasion and induces apoptosis by regulating the expression of WNT1 via miR-637 in colorectal cancer.

Colorectal cancer (CRC) is a common malignancy. Sevoflurane has been reported to involve in the progression in several cancers. However, the molecular mechanism of sevoflurane in CRC progression remains unclear. Quantitative real-time PCR and western blot was used to detect the expression of miR-637 and WNT1. Cell migration, invasion and apoptosis were detected by transwell assay, flow cytometry or western blot, respectively. The interaction between WNT1 and miR-637 was confirmed by luciferase reporter assay, RNA immunoprecipitation assay and pull-down assay. We found sevoflurane could inhibit cell migration and invasion but induced apoptosis in CRC. Besides, the miR-637 level was decreased in CRC tissues and cells but could be rescued by sevoflurane. MiR-637 overexpression enhanced the anticancer functions of sevoflurane in CRC cells, while miR-637 inhibition showed opposite effects. WNT1 was confirmed to be a target of miR-637 and was inhibited by sevoflurane or miR-637. Importantly, knockdown of WNT1 reversed the carcinogenic effects mediated by miR-637 inhibitor in CRC cells treated with sevoflurane. Collectively, sevoflurane inhibited cell migration, invasion and induced apoptosis by regulating the miR-637/WNT1 axis in colorectal cancer, indicating a novel insight into the effective clinical implication for the anesthetic in CRC treatment.