AKT1 and neoplasm: Furthermore, knockdown of AKT1 expression abolished effects of miR-149 overexpression in HepG2 cells, including inhibiting cell proliferation (Figure 6C), invasion (Figure 6D) and migration (Figure 6E), indicating that the tumor suppressive roles of miR-149 in HCC were partially mediated by targeting AKT1-mTOR pathway.