Magnitude of Peroxisome Proliferator-Activated Receptor-γ Activation is Associated With Important and Seemingly Opposite Biological Responses in Breast Cancer Cells

BackgroundThe nuclear receptor peroxisome proliferator-activated receptor-γ (PPARγ) has become a potential target for the prevention and treatment of breast cancer. However, recent in vitro and in vivo studies have raised the question of whether activation of PPARγ leads to the promotion or reductio...

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Published in:Journal of investigative medicine 2001-09, Vol.49 (5), p.413-420
Main Authors: Clay, Carl E., Namen, Andrew M., Atsumi, Gen-ichi, Trimboli, Anthony J., Fonteh, Alfred N., High, Kevin P., Chilton, Floyd H.
Format: Article
Language:English
Subjects:
Apoptosis - drug effects
Breast Neoplasms - pathology
Cell Cycle - drug effects
Cell Differentiation - drug effects
Cell Division - drug effects
Chromans - pharmacology
Female
Humans
Prostaglandin D2 - analogs & derivatives
Prostaglandin D2 - pharmacology
Receptors, Cytoplasmic and Nuclear - physiology
Thiazoles - pharmacology
Thiazolidinediones
Transcription Factors - physiology
Transcriptional Activation - drug effects
Tumor Cells, Cultured
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Summary:BackgroundThe nuclear receptor peroxisome proliferator-activated receptor-γ (PPARγ) has become a potential target for the prevention and treatment of breast cancer. However, recent in vitro and in vivo studies have raised the question of whether activation of PPARγ leads to the promotion or reduction of tumor formation. Studies using several cancer cell lines, animal models, and a variety of PPARγ agonists have shown discordant results, including changes in cellular proliferation, differentiation, and apoptosis of cancer cells and tumors.MethodsWe studied the effects of low-, moderate-, and high-dose treatment of the PPARγ ligands 15-deoxy-Δ12,14 prostaglandin J2 (15dPGJ2) and troglitazone (TGZ) on parameters of cell growth, differentiation, and apoptosis in the epithelial breast cancer cell line MDA-MB-231.ResultsThe biologic effects of these compounds depend largely on ligand concentration and the degree of PPARγ activation. For example, low concentrations of 15dPGJ2 (
ISSN:1081-5589
1708-8267
DOI:10.2310/6650.2001.33786