TY - JOUR
T1 - The non-genomic crosstalk between PPAR-γ ligands and ERK1/2 in cancer cell lines
AU - Papageorgiou, Efstathia
AU - Pitulis, Nea
AU - Msaouel, Pavlos
AU - Lembessis, Peter
AU - Koutsilieris, Michael
N1 - Copyright:
Copyright 2009 Elsevier B.V., All rights reserved.
PY - 2007
Y1 - 2007
N2 - Peroxisome proliferator activated receptors (PPARs) are members of the nuclear receptor superfamily acting as transcription factors. PPAR-γ, one of the three PPAR subtypes, is expressed in many malignant and non-malignant cells and tissues. PPAR-γ ligands influence cancer biology via both genomic as well as non-genomic events. The non-genomic action of PPAR-γ ligands, including the activation of MAPK signaling pathways, is under intense investigation. In the presence of PPAR-γ 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-γ transcriptional activity by phosphorylation. This paper reviews the interrelation of PPAR-γ ligands and activated ERK1/2, in relation to their antineoplastic actions in cancer cell lines, which may offer the potential for improved anticancer therapies.
AB - Peroxisome proliferator activated receptors (PPARs) are members of the nuclear receptor superfamily acting as transcription factors. PPAR-γ, one of the three PPAR subtypes, is expressed in many malignant and non-malignant cells and tissues. PPAR-γ ligands influence cancer biology via both genomic as well as non-genomic events. The non-genomic action of PPAR-γ ligands, including the activation of MAPK signaling pathways, is under intense investigation. In the presence of PPAR-γ 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-γ transcriptional activity by phosphorylation. This paper reviews the interrelation of PPAR-γ ligands and activated ERK1/2, in relation to their antineoplastic actions in cancer cell lines, which may offer the potential for improved anticancer therapies.
KW - Cancer
KW - ERK1/2
KW - Non-genomic effects
KW - PPAR-γ
KW - Thiazolidinedione
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U2 - 10.1517/14728222.11.8.1071
DO - 10.1517/14728222.11.8.1071
M3 - Review article
C2 - 17665979
AN - SCOPUS:34547792266
SN - 1472-8222
VL - 11
SP - 1071
EP - 1085
JO - Expert Opinion on Therapeutic Targets
JF - Expert Opinion on Therapeutic Targets
IS - 8
ER -