Fig. 8
The MnSOD/FoxM1 axis is a novel target for isovitexin-associated inhibition of carcinogenicity and stemness in HCSLCs from HepG2 and SMMC-7721 cells a Immunoblotting for MnSOD and FoxM1 expression levels in HepG2 and SMMC-7721 cells and respective HCSLCs, with β-actin antibodies as a loading control; b and c Sphere and colony formation rates in HepG2 and SMMC-7721 cells and respective HCSLCs. d Immunoblotting for determining CK133, CD44 and ALDH1 expression level in HepG2 and SMMC-7721 cells and respective HCSLCs, with β-actin as an internal control. Data are mean ± SD (n = 3); P < 0.05 indicated statistical significance. * HepG2 cells. #SMMC-7721 cells. e Immunoblotting for assessing MnSOD and FoxM1 expression levels in HCSLCs from HepG2 and SMMC-7721 cells incubated with or without isovitexin (ISOV; 10 μM). Data are mean ± SD (n = 3); P < 0.05 indicated statistical significance. * Vehicle control in HCSLCs from HepG2 cells. #Vehicle control in HCSLCs from SMMC-7721 cells. f Schematic diagram of the mechanism underlying isovitexin inhibits HCSLC carcinogenicity and stemness via the MnSOD/FoxM1 axis. Isovitexin effectually inhibited carcinogenicity and stemness in HCSLCs by downregulating FoxM1 likely through preventing MnSOD overexpression induced mitochondrial H2O2-mediated an increased binding of E2F1 and Sp1 onto FoxM1 promoter