Cucurbitane Triterpenoid from Momordica charantia Induces Apoptosis and Autophagy in Breast Cancer Cells, in Part, through Peroxisome Proliferator-Activated Receptor γ Activation
Figure 3
The PPARγ-inducing activity of DMC. (a) Dose-dependent effect of DMC on PPARγ activation in MCF-7 cells. Cells were transfected with PPRE x3-TK-Luc and Renilla plasmids for 24 h before treatment with DMC at indicated concentrations for 24 h. Data are expressed as percentage of the respective PPARγ activity to the control. Normalized luciferase activity was determined and is shown as the fold activation relative result in DMSO-treated cells. Troglitazone at 50 μM was used as positive control. Values are means ± S.E.M. of three independent experiments. . (b) DMC-inhibited cell growth could be blocked by GW9662, an inhibitor of PPARγ. Cells were treated with DMC at indicated concentrations in the presence of 5 μM GW9662 or DMSO control for 72 h, and cell viability was determined by MTT assays. Points, mean; bars, SD (). , . (c) Effect of DMC on the protein expression and nuclear translocation of PPARγ. MCF-7 cells were treated with DMC at the indicated concentrations for 72 h and detected PPARγ by Western blotting (upper panel). MCF-7 cells were treated with 10 μM DMC or 10 μM troglitazone (TG) for 24 h, stained with anti-PPARγ, and examined by confocal microscopy (lower panel). (d) Dose-dependent effect of DMC on the expression of various PPARγ-targeted proteins in MCF-7 cells after 72 h exposure in 5% FBS-supplemented DMEM/F12 medium.
