A Ligand for Peroxisome Proliferator-Activated Receptor γ Inhibits Human Cholangiocarcinoma Cell Growth: Potential Molecular Targeting Strategy for Cholangioma

2006 ◽  
Vol 51 (9) ◽  
pp. 1650-1657 ◽  
Author(s):  
T. Kobuke ◽  
S. Tazuma ◽  
H. Hyogo ◽  
K. Chayama
Keyword(s):  
Cell Growth ◽  
Growth Potential ◽  
Molecular Targeting ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Cholangiocarcinoma Cell ◽  
Targeting Strategy

Activation of peroxisome proliferator-activated receptor-γ by troglitazone (TGZ) inhibits human lung cell growth

2005 ◽  
Vol 96 (4) ◽  
pp. 760-774 ◽  
Author(s):  
Mingyue Li ◽  
Tak W. Lee ◽  
Tony S.K. Mok ◽  
Timothy D. Warner ◽  
Anthony P.C. Yim ◽  
...  
Keyword(s):  
Cell Growth ◽  
Human Lung ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor

Cotreatment with Pioglitazone, a Synthetic Ligand for Peroxisome Proliferator-Activated Receptor γ (PPARγ), Enhances Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL)-Induced Apoptosis of Human Leukemia Cells.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 4377-4377
Author(s):  
Joo-In Park ◽  
Hoon Han ◽  
Ji-Seon Han ◽  
Hyuk-Chan Kwon ◽  
Jin-Yeong Han ◽  
...  
Keyword(s):  
Cell Growth ◽  
Cell Line ◽  
Myeloid Cell ◽  
Leukemia Cells ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Myeloid Cell Line ◽  
Synthetic Ligand ◽  
Induced Apoptosis ◽  
Acute Myeloid

Abstract Imatinib (STI571, Glivec) is the choice treatment for Bcr/Abl-positive malignancies. Emergence of resistance to Imatinib warrants the exploration of novel well-tolerated anticancer agents. Peroxisome proliferator-activated receptor γ (PPARγ) is a nuclear receptor family, which mainly associates with the adipocyte differentiation, but also appears to facilitate cell differentiation or apoptosis in certain malignant cells. Previous studies imply that the PPARγ activation pathway may be a possible intervention mode for treatment of leukemia, which is resistant to imatinib (STI571). In this study, we investigated the effects of pioglitazone, a synthetic ligand for PPARg, on the cell growth and TRAIL-induced apoptosis in a novel imatinib (STI571) resistant acute myeloid cell line (SR-1), which we have established from an STI571 resistant blast crisis patient, as well as HL-60 cells. HL-60 and SR-1 cells are relatively resistant to TRAIL-induced apoptosis. Pioglitazone alone inhibited the cell growth of SR-1 and HL-60 cells, but did not induce the apoptosis of these cell lines. However, simultaneous exposure of cells to 100 ng/ml TRAIL with either 25 μM pioglitazone or 50 μM piogliazone resulted in a striking increase in apoptosis. To clarify the mechanism of pioglitazone to sensitize the leukemia cells to TRAIL-induced apoptosis, we investigated the change of the proteins related to cell cycle and apoptosis by western blot. As results, we observed the significant decrease of X-linked inhibitor of apoptosis (XIAP) and the increased expression of p21 by cotreatment of pioglitazone with TRAIL. Taken together, these findings indicate that pioglitazone may have promising activity in augmenting TRAIL-induced apoptosis of human acute leukemia cells including the imatinib (STI571) resistant acute myeloid cell line.

scholarly journals Ligand activation of peroxisome proliferator-activated receptor-β/δ(PPARβ/δ) inhibits cell growth of human N/TERT-1 keratinocytes

2007 ◽  
Vol 19 (6) ◽  
pp. 1163-1171 ◽  
Author(s):  
Andrew D. Burdick ◽  
Moses T. Bility ◽  
Elizabeth E. Girroir ◽  
Andrew N. Billin ◽  
Timothy M. Willson ◽  
...  
Keyword(s):  
Cell Growth ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ligand Activation
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