Sevoflurane Confers Protection Against the Malignant Phenotypes of Lung Cancer Cells via the microRNA-153-3p/HIF1α/KDM2B Axis

Sevoflurane is shown to curtail lung cancer (LC) development. Herein, this research sought to investigate the underlying mechanism of sevoflurane in regard to its repressive effects on LC. Expression levels of microRNA (miR)-153-3p, HIF1 alpha, and KDM2B in LC tissues and cells were determined with qRT-PCR. Following sevoflurane pretreatment and/or ectopic expression and knockdown experiments, the malignant phenotypes, and levels of miR-153-3p, HIF1 alpha, and KDM2B in LC A549 cells were detected using Transwell, scratch, EdU, CCK-8, Western blot, and qRT-PCR assays. Relationship between HIF1 alpha and miR-153-3p was verified with a dual-luciferase reporter assay. The interaction between HIF1 alpha and KDM2B was verified with a ChIP assay. LC tissues and cells presented low miR-153-3p expression and high HIF1 alpha and KDM2B expression. Sevoflurane pretreatment, miR-153-3p upregulation, HIF1 alpha downregulation, or KDM2B downregulation impeded the malignant phenotypes of A549 cells. Sevoflurane pretreatment augmented miR-153-3p expression, while miR-153-3p negatively targeted HIF1 alpha. HIF1 alpha bound to the KDM2B promoter to upregulate KDM2B. HIF1 alpha or KDM2B overexpression counteracted the inhibitory effects of sevoflurane pretreatment on A549 cell malignant behaviors. Sevoflurane decreased HIF1 alpha expression through upregulation of miR-153-3p, thereby reducing KDM2B transcription to restrict the malignant phenotypes of LC A549 cells.