scholarly journals Inhibition of adult liver progenitor (oval) cell growth and viability by an agonist of the peroxisome proliferator activated receptor (PPAR) family member γ, but not α or δ

2005 ◽  
Vol 26 (10) ◽  
pp. 1782-1792 ◽  
Author(s):  
Belinda Knight ◽  
Bu B. Yeap ◽  
George C. Yeoh ◽  
John K. Olynyk
Keyword(s):  
Cell Growth ◽  
Family Member ◽  
Peroxisome Proliferator ◽  
Oval Cell ◽  
Adult Liver ◽  
Peroxisome Proliferator Activated Receptor ◽  
Cell Growth And Viability

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

Differential cell growth/apoptosis behavior of 13-hydroxyoctadecadienoic acid enantiomers in a colorectal cancer cell line

2014 ◽  
Vol 307 (6) ◽  
pp. G664-G671 ◽  
Author(s):  
Marisol Cabral ◽  
Raquel Martín-Venegas ◽  
Juan José Moreno
Keyword(s):  
Cell Growth ◽  
Dna Synthesis ◽  
Cancer Cell Line ◽  
Colorectal Cancer Cell Line ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Proliferative Effect ◽  
Pathway Activation ◽  
Apoptotic Effect ◽  
Fetal Bovine

Cyclooxygenases (COXs) and lipoxygenases (LOXs) are important enzymes that metabolize arachidonic and linoleic acids. Various metabolites generated by the arachidonic acid cascade regulate cell proliferation, apoptosis, differentiation, and senescence. Hydroxyoctadecadienoic acids (HODEs) are synthesized from linoleic acid, giving two enantiomeric forms for each metabolite. The aim was to investigate the effect of 13-HODE enantiomers on nondifferentiated Caco-2 cell growth/apoptosis. Our results indicate that 13(S)-HODE decreases cell growth and DNA synthesis of nondifferentiated Caco-2 cells cultured with 10% fetal bovine serum (FBS). Moreover, 13(S)-HODE showed an apoptotic effect that was reduced in the presence of a specific peroxisome proliferator-activated receptor-γ (PPARγ) antagonist. In addition, we observed that 13(S)-HODE but not 13(R)-HODE is a ligand to PPARγ, confirming the implication of this nuclear receptor in 13(S)-HODE actions. In contrast, 13(R)-HODE increases cell growth and DNA synthesis in the absence of FBS. 13(R)-HODE interaction with BLT receptors activates ERK and CREB signaling pathways, as well as PGE2 synthesis. These results suggest that the proliferative effect of 13(R)-HODE could be due, at least in part, to COX pathway activation. Thus both enantiomers use different receptors and have contrary effects. We also found these differential effects of 9-HODE enantiomers on cell growth/apoptosis. Therefore, the balance between (R)-HODEs and (S)-HODEs in the intestinal epithelium could be important to its cell growth/apoptosis homeostasis.

scholarly journals Role of Peroxisome Proliferator-Activated Receptor Alpha in the Control of Cyclooxygenase 2 and Vascular Endothelial Growth Factor: Involvement in Tumor Growth

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-10 ◽  
Author(s):  
Raquel Grau ◽  
Manuel D. Díaz-Muñoz ◽  
Cristina Cacheiro-Llaguno ◽  
Manuel Fresno ◽  
Miguel A. Iñiguez
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cell Growth ◽  
Tumor Growth ◽  
Peroxisome Proliferator ◽  
Vascular Endothelial ◽  
Peroxisome Proliferator Activated Receptor ◽  
Cox 2 ◽  
Endothelial Growth Factor

A growing body of evidence indicates that PPAR (peroxisome proliferator-activated receptor)αagonists might have therapeutic usefulness in antitumoral therapy by decreasing abnormal cell growth, and reducing tumoral angiogenesis. Most of the anti-inflammatory and antineoplastic properties of PPAR ligands are due to their inhibitory effects on transcription of a variety of genes involved in inflammation, cell growth and angiogenesis. Cyclooxygenase (COX)-2 and vascular endothelial growth factor (VEGF) are crucial agents in inflammatory and angiogenic processes. They also have been significantly associated to cell proliferation, tumor growth, and metastasis, promoting tumor-associated angiogenesis. Aberrant expression of VEGF and COX-2 has been observed in a variety of tumors, pointing to these proteins as important therapeutic targets in the treatment of pathological angiogenesis and tumor growth. This review summarizes the current understanding of the role of PPARαand its ligands in the regulation of COX-2 and VEGF gene expression in the context of tumor progression.

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