PPARγ ligands inhibit primary tumor growth and metastasis by inhibiting angiogenesis
Dipak Panigrahy, Samuel Singer, Lucy Q. Shen, Catherine E. Butterfield, Deborah A. Freedman, Emy J. Chen, Marsha A. Moses, Susan Kilroy, Stefan Duensing, Christopher Fletcher, Jonathan A. Fletcher, Lynn Hlatky, Philip Hahnfeldt, Judah Folkman, Arja Kaipainen
Dipak Panigrahy, Samuel Singer, Lucy Q. Shen, Catherine E. Butterfield, Deborah A. Freedman, Emy J. Chen, Marsha A. Moses, Susan Kilroy, Stefan Duensing, Christopher Fletcher, Jonathan A. Fletcher, Lynn Hlatky, Philip Hahnfeldt, Judah Folkman, Arja Kaipainen
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PPARγ ligands inhibit primary tumor growth and metastasis by inhibiting angiogenesis

Abstract

Research Article

Authors

Dipak Panigrahy, Samuel Singer, Lucy Q. Shen, Catherine E. Butterfield, Deborah A. Freedman, Emy J. Chen, Marsha A. Moses, Susan Kilroy, Stefan Duensing, Christopher Fletcher, Jonathan A. Fletcher, Lynn Hlatky, Philip Hahnfeldt, Judah Folkman, Arja Kaipainen

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TZDs activate endothelial PPARγ in a lactacystin-reversible manner. (a) ...
TZDs activate endothelial PPARγ in a lactacystin-reversible manner. (a) Western blot analysis of PPARγ protein in proliferating HUVECs. PPARγ protein levels decrease in a dose-dependent manner with rosiglitazone (Rosi). Control, C3H/10T 1/2 (fully differentiated C3H cells), a positive control for PPARγ; –, HUVECs cultured in starvation media; +, HUVECs cultured in stimulation (growth) media. (b) PPARγ protein decreases with 5 μM (5T) and 10 μM (10T) troglitazone. In contrast, PPARα activator WY 14643 at 5 μM (5W) has no effect. 1R, 1 μM concentration of rosiglitazone. (c) PPARγ activation can be reversed by coadministration of 2.5 μM lactacystin. HUVECs treated with both rosiglitazone and lactacystin (lanes 3 and 5) show PPARγ expression comparable to that of HUVECs treated with stimulation medium alone (lane 1). Lactacystin alone has no effect on basal PPARγ levels (lane 6).