Fig. 4

PTTG1 knock-out and FoxM1 knock-down suppress colon cancer cell migration, invasion and liver metastasis. a, b In vitro migration (a) and invasion (b) assays in HCT116 cells. Left panel: representative migration and invasion photographs of PTTG1^+/+, PTTG1^−/−, control siRNA- and FoxM1 siRNA (siFoxM1)-transfected cells. Right panel: quantification of migrated and invaded cells per field at × 40 magnification. Experiments were repeated three times. c Wound-healing assay in FoxM1 over expressing PTTG1^+/+ and PTTG1^−/− HCT116 cells. The cells were allowed to form monolayers in a 6-well plate. A wound was created by a pipette tip. The healing of the wounds was monitored under microscope. Pictures were taken at different time points. Left panel: representative migration images of FoxM1 over expressing PTTG1^+/+ and PTTG1^−/− HCT116 cells. Right panel: wound closure percentage was determined by subtracting values obtained at 0 h from 24 h. Experiments were repeated three times. d FoxM1 over expressing PTTG1^+/+ or PTTG1^−/− HCT116 cells were injected into spleen to induce liver metastasis. Left panel: representative images of metastatic liver tumor derived from mice injected with control cells and FoxM1 overexpressing cells. Histochemistry and western blots indicated that the metastatic foci are derived from the injected cells and FoxM1 was overexpressed in the FoxM1 overexpressing group. Right panel: summary of metastatic liver foci numbers and liver weight. All data above are presented as the mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001