The non-genomic crosstalk between PPAR-γ ligands and ERK1/2 in cancer cell lines

被引：40

作者：

Papageorgiou, Efstathia ^{[1
]}

Pitulis, Nea ^{[1
]}

Msaouel, Pavlos ^{[1
]}

Lembessis, Peter ^{[1
]}

Koutsilieris, Michael ^{[1
]}

机构：

[1] Natl & Kapodistrian Univ Athens, Dept Expt Physiol, Med Sch, Athens 11527, Greece

来源：

EXPERT OPINION ON THERAPEUTIC TARGETS | 2007年 / 11卷 / 08期

关键词：

cancer; ERK1/2; non-genomic effects; PPAR-7; thiazolidinedione;

D O I：

10.1517/14728222.11.8.1071

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Peroxisome proliferator activated receptors (PPARs) are members of the nuclear receptor superfamily acting as transcription factors. PPAR-gamma, one of in the three PPAR subtypes, is expressed in many malignant and non-malignant cells and tissues. PPAR-gamma, ligands influence cancer biology via both genomic as well as non-genomic events. The non-genomic action of PPAR-gamma ligands, including the activation of MAPK signaling pathways, is under intense investigation. In the presence of PPAR-gamma ligands, a rapid phosphorylation of ERK1/2 is observed in many cancer cell lines. Activated ERK1/2 elicits rapid, non-genomic cellular effects and can directly repress PPAR-gamma transcriptional activity by phosphorylation. This paper reviews the interrelation of PPAR-gamma ligands and activated ERK1/2, in relation to their antineoplastic actions in cancer cell lines, which may offer the potential for improved anticancer therapies.

引用

页码：1071 / 1085

页数：15

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