Troglitazone, a peroxisome proliferator-activated receptor γ ligand, induces growth inhibition and apoptosis of HepG2 human liver cancer cells

Figure 1 Effect of troglitazone on growth of HepG2 cells. Cells were incubated with different concentrations of troglitazone for 120 h. Troglitazone inhibited growth of HepG2 cells in a dose-dependent manner, as demonstrated by MTT assay. Data represent the mean ± SD from six wells. ^bP < 0.01 vs corresponding control group (unpaired Student’s t test).

Figure 2 Morphological changes were examined by phase-contrast microscopy. A:Controls; B: 30 &mgr;mol/L troglitazone.

Figure 3 Cell cycle analysis by flow cytometry. A: Control cells; B: 20 &mgr;mol/L troglitazone; C: 30 &mgr;mol/L troglitazone.

Figure 4 Troglitazone significantly increased the number of TUNEL-positive cells in a dose-dependent manner. A: Control cells; B: 20 &mgr;mol/L troglitazone; C: 30 &mgr;mol/L troglitazone.

Figure 5 Immunocytochemistry showed that caspase-3 was activated. The shrunken cells were positively stained for activated caspase-3. No positive cell was detectable in the control group ( A: original magnification, × 200). Whereas large numbers of positive cells labeled for activated caspase-3 were observed in HepG2 cells treated with 30 &mgr;mol/L troglitazone for 24 h ( B: original magnification, × 400).

Figure 6 Survivin was present predominantly in the nucleus in untreated cells ( A: original magnification, × 400) as demonstrated by immunocytochemistry. After exposure of HepG2 cells to 30 &mgr;mol/L troglitazone for 24 h, survivin incompletely translocated from the nucleus to the cytoplasma ( B: original magnification, × 400).

Figure 7 Effect of troglitazone on the expression of Bax and survivin. Lane 1: Control cells; lane 2: 20 &mgr;mol/L troglitazone; lane 3: 30 &mgr;mol/L troglitazone.