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

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.

Thiazolidinedione (TZD) exposure and risk of squamous cell carcinoma of head and neck (SCCHN)

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 1511-1511 ◽  
Author(s):  
R. Govindarajan ◽  
E. R. Siegel ◽  
D. L. Simmons ◽  
N. P. Lang
Keyword(s):  
Cox Regression ◽  
Veterans Affairs ◽  
Time Dependent ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ligand Activation ◽  
Hazard Ratios ◽  
Patient Database ◽  
Time Dependent Covariates ◽  
Va Health Care System

1511 Background: Peroxisome proliferator-activated receptor γ (PPARγ), a nucleic acid receptor, heterodimerizes with retinoic acid X receptor (RXR). Ligand activation of RXR leads to decreased proliferation of SCCHN cell lines. TZDs (syn: glitazones), used to treat diabetes mellitus (DM), are ligands for the RXR:PPARγ heterodimer. A retrospective study of diabetics attending the Veterans Affairs (VA) health care system was undertaken to assess the association between TZD exposure and the risk of developing SCCHN. Methods: Data were obtained from the electronic patient database VISN 16 (covering 10 VA institutions) for males aged ≥40 presenting with DM and no prior SCCHN between 10/01/96 and 12/31/03. DM and SCCHN diagnoses were identified using ICD9 codes. Subjects were followed until 12/31/05, and analyzed for SCCHN risk via Cox regression, using time-dependent covariates to model exposure to TZDs, insulin and other anti-DM agents. Results: 130,406 subjects met the study criteria. Median (quartiles) age at DM presentation was 64 (55–72).18.5% were African-American, 61.3% were Caucasian, and 20.2% were other/unknown. The table shows TZD exposure, SCCHN incidence and hazard ratios for SCCHN with exposure to TZD alone or in combination with insulin and other anti-DM agents after adjusting for age, race, BMI, and HbA1C. Conclusions: A 41%-55% reduction in the risk of SCCHN was observed in diabetic subjects treated with TZD alone, with insulin, and with other anti-DM agents. The decrease was statistically significant (P<0.05) for TZD alone and TZD with other agents, but not for TZD with insulin. These findings suggest a protective effect of TZD on the development of SCCHN. The mechanism is not clearly known but possibly mediated through RXR:PPARγ pathway. [Table: see text] No significant financial relationships to disclose.

Sign in / Sign up

Export Citation Format

Share Document