The PPAR Gamma Agonist Troglitazone Regulates Erk 1/2 Phosphorylation via a PPARγ-Independent, MEK-Dependent Pathway in Human Prostate Cancer Cells
Figure 4
U0126 does not alter the transcriptional activity of PPARγ in prostate cancer cells. PC-3 cells were plated in 6-wells plates and transfected with the PPRE-luciferase and CMV β-galactosidase reporter plasmids. The transfected cells were then treated for twenty-four hours with DMSO vehicle or troglitazone (2.5–40 μM) in the presence or absence of 10 μM U0126. 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 μM U0126, 0 μM troglitazone). At each concentration of troglitazone tested, there was no statistically significant difference noted between the troglitazone and troglitazone + U0126 groups. A representative experiment is shown.
