Antineoplastic effects of peroxisome proliferatoractivated receptor γ agonists
2004; Elsevier BV; Volume: 5; Issue: 7 Linguagem: Inglês
10.1016/s1470-2045(04)01509-8
ISSN1474-5488
AutoresChristian Grommes, Gary E. Landreth, Michael T. Heneka,
Tópico(s)Genomics, phytochemicals, and oxidative stress
ResumoPeroxisome proliferator-activated receptors (PPAR) are members of a superfamily of nuclear hormone receptors. Activation of PPAR isoforms elicits both antineoplastic and anti-inflammatory effects in several types of mammalian cells. PPARs are ligand-activated transcription factors and have a subfamily of three different isoforms: PPARα, PPARγ, and PPARβ/δ. All isoforms heterodimerise with the 9-cisretinoic acid receptor RXR, and play an important part in the regulation of several metabolic pathways, including lipid biosynthesis and glucose metabolism. Endogenous ligands of PPARγ include long-chain polyunsaturated fatty acids, eicosanoid derivates, and oxidised lipids. Newly developed synthetic ligands include thiazolidinediones—a group of potent PPARγ agonists and antidiabetic agents. Here, we review PPARγ-induced antineoplastic signalling pathways, and summarise the antineoplastic effects of PPARγ agonists in different cancer cell lines, animal models, and clinical trials.
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