Moreover, wound-healing assays also demonstrated that overexpression of miR-149 could markedly reduce the migration activities of HepG2 cells (P = 0.01, Figure 5D and E).To further verify whether the role of miR-149 in tumorigenesis of HCC was mediated via targeting AKT1-mTOR signaling, AKT1 expression in HepG2 cells was knockdown via siRNA, which resulted in the downregulation of AKT1, p-AKT1, mTOR and mTOR proteins (Figure 6A and B). This evidence concerns the gene AKT1 and hepatocellular carcinoma.