期刊
TOXICOLOGY
卷 243, 期 1-2, 页码 236-243出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.tox.2007.10.023
关键词
peroxisome proliferator-activated receptor; melanoma; breast cancer; nuclear receptor; cell proliferation
资金
- NCI NIH HHS [R01 CA124533, R01 CA097999-05, CA124533, R01 CA097999, CA97999, R01 CA124533-01] Funding Source: Medline
The development of peroxisome proliferator-activated receptor-beta/delta (PPAR beta/delta) ligands for the treatment of diseases including metabolic syndrome, diabetes and obesity has been hampered due to contradictory findings on their potential safety. For example, while some reports show that ligand activation of PPAR beta/delta promotes the induction of terminal differentiation and inhibition of cell growth, other reports suggest that PPAR beta/delta ligands potentiate tumorigenesis by increasing cell proliferation. Some of the contradictory findings could be due in part to differences in the ligand examined, the presence or absence of serum in cell cultures, differences in cell lines or differences in the method used to quantify cell growth. For these reasons, this study examined the effect of ligand activation of PPAR beta/delta on cell growth of two human cancer cell lines, MCF7 (breast cancer) and UACC903 (melanoma) in the presence or absence of serum using two highly specific PPAR beta/delta ligands, GW0742 or GW501516. Culturing cells in the presence of either GW0742 or GW501516 caused upregulation of the known PPAR beta/delta target gene angiopoiefin-like protein 4 (ANGPTL4). Inhibition of cell growth was observed in both cell lines cultured in the presence of either GW0742 or GW501516, and the presence or absence of serum had little influence on this inhibition. Results from the present studies demonstrate that ligand activation of PPAR beta/delta inhibits the growth of both MCF7 and UACC903 cell lines and provide further evidence that PPAR beta/delta ligands are not mitogenic in human cancer cell lines. Published by Elsevier Ireland Ltd.
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