The PPAR Gamma Agonist Troglitazone Regulates Erk 1/2 Phosphorylation via a PPARγ-Independent, MEK-Dependent Pathway in Human Prostate Cancer Cells
Figure 3
Troglitazone-stimulated increases in Erk phosphorylation occur independently of PPARγ. (a) PC-3 cells were treated for 30 minutes or two hours with DMSO vehicle control (D) or the PPARγ ligands troglitazone (T; 40 μM), rosiglitazone (R; 40 μM), or pioglitazone (P; 30 μM). The level of ERK 1/2 (both total and phosphorylated) and actin was then detected by Western blot analysis. (b) PC-3 cells were first transfected with the PPRE-luciferase and CMV-β-galactosidase reporter plasmids. Cells were then treated for 24 hours with DMSO vehicle or troglitazone (10 or 40 μM) in the presence or absence of the PPARγ antagonist GW9662 (10 μM). The level of luciferase activity in treated cells was measured and normalized to β-galactosidase activity. Each bar represents the mean SD for three wells. * compared to vehicle control (0 Trog, − GW9662). (c) PC-3 cells were treated for two hours with DMSO vehicle (−) or 40 μM troglitazone (+) in the presence or absence of the MEK inhibitor U0126 (10 μM) or the PPARγ antagonist GW9662 (10 μM). Western blotting was then used to measure Erk and actin levels within treated cells. The data from each blot were quantified and expressed relative to the signal present in the vehicle control sample (−Trog, −U0126, −GW9662).
