Figure 1

The effects of PPARγ ligands on PC-3 cell metabolism, growth, and apoptosis. (A) The dose-dependent effect of rosiglitazone (ROS) and 15dPGJ2 on PC-3 cell metabolism/growth as assessed by MTT assay. Note that the increasing concentrations of the ROS (0 µM to 50 µM) and of 15dPGJ2 (0 µM to 10 µM) resulted in a dose-dependent inhibition of the PC-3 cell metabolism/growth after 96 h incubation with the respective drug. A 50% inhibition of metabolism/growth of PC-3 cells was evident at concentrations of 2 µM of 15dPGJ2 and 10 µM of rosiglitazone. Results are expressed as percentage of controls in triplicate experiments. (B) Dose-dependent and time-dependent inhibition of PC-3 cell growth as assessed by Trypan blue exclusion assays. Note that ROS (1 µM and 10 µM) and 15dPGJ2 (2 µM and 5 µM) inhibited the number of living PC-3 cells in a time-dependent and dose-dependent manner (24 and 48 h). (C) An example of the PPARγ-induced apoptosis of PC-3 cells as assessed by flow cytometry (96 h incubation using AnnexinV-FITC and PI staining as described in Materials and Methods). ROS and 15dPGJ2 did not produce evidence of apoptosis of PC-3 cells under these experimental conditions. Percentage (%) of alive PC-3 cells distributed within the cell cycle: control = 89.5; ROS = 85.8; 15dPGJ2 = 88.4. (D) In this panel the results of apoptosis data of flow cytometry in triplicate experiments are expressed as number of apoptotic cells (%) compared with total cell number. Statistical analysis was performed by Student ttest. Values are means ± SD (P < 0.05).