Fig. 7

PPAR-γ/AKT signaling is essential for the biological function of miR-1468 in HCC. a Hep3B and MHCC-97 L cells that were transfected with corresponding miRNA vectors were subjected to immunoblotting for phosphorylated AKT and AKT. PPAR-γ agonist rosiglitazone treatment inhibited the promotive effects on cell proliferation (b, c), colony formation (d), cell cycle progression (e) and apoptosis (f) of miR-1468 overexpressing Hep3B cells. PPAR-γ antagonist, T0070907, reversed the suppressive effects of miR-1468 knockdown in MHCC-97 L cells. g Western blot analysis indicated that modulating PPAR-γ activation reversed the effects of miR-1468 alteration on cell cycle and apoptosis associated factors of HCC cells. *P < 0.05