Sevo exerts its antitumor effects by blocking the PTEN/Akt/GSK-3β/β-catenin signaling pathway through the downregulation of miR-25-3p in hepatocellular carcinoma cells. HCCLM3 and Huh7 cells were treated with 1 µM PI3K inhibitor LY294002 or 100 ng/ml PI3K signaling activator insulin-like growth factor-1 for 24 h followed by Sevo treatment for 6 h. (A) Cell proliferation was determined by MTT assay. (B) Cell invasion was measured by Transwell assay. (C) Cell migration was detected by wound healing assay. Data are the mean ± standard deviation. (n=3) of three representative experiments, *P<0.01 and **P<0.01 vs. negative control group. #P<0.05 vs. Sevo, &&P<0.01 vs. Sevo. Sevo, sevoflurane; NC, negative control; miR/miRNA, microRNA; OD, optical density; PTEN, phosphatidylinositol 3,4,5-trisphosphate 3-phosphatase and dual-specificity protein phosphatase PTEN;GSK, glycogen synthase kinase; p-Akt, phosphorylated-protein kinase B; PI3K, phosphatidylinositol 3 kinase.