Fig. 3

APE1 stimulates EMT and invasion through a redox-dependent mechanism in cervical cancer cells. a APX3330, an APE1 redox inhibitor, increased E-cadherin but inhibited N-cadherin and vimentin expression in cervical cancer cells. The indicated cells were treated with DMSO or 5 μM APEX3330 for 24 h and then subjected to western blot analysis. b Treatment of cervical cancer cells with APE1 inhibitor III did not affect EMT marker protein expression in cervical cancer cells. Cells were treated with DMSO or 7.5 μM APE1 inhibitor III for 24 h and then subjected to western blot analysis. c APE1 C65S, a mutant that ablates APE1 redox function, inhibited EMT compared to wild-type APE1. Western blotting was performed 72 h post-transfection. d Cervical cancer cell invasion was inhibited by APX3330 but not by APE1 inhibitor III. *, P < 0.05; **, P < 0.01; ***, P < 0.001