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Medientyp:
E-Artikel
Titel:
PPARγ and MEK Interactions in Cancer
Beteiligte:
Burgermeister, Elke;
Seger, Rony
Erschienen:
Wiley, 2008
Erschienen in:
PPAR Research, 2008 (2008) 1
Sprache:
Englisch
DOI:
10.1155/2008/309469
ISSN:
1687-4757;
1687-4765
Entstehung:
Anmerkungen:
Beschreibung:
Peroxisome proliferator‐activated receptor‐gamma (PPARγ) exerts multiple functions in determination of cell fate, tissue metabolism, and host immunity. Two synthetic PPARγ ligands (rosiglitazone and pioglitazone) were approved for the therapy of type‐2 diabetes mellitus and are expected to serve as novel cures for inflammatory diseases and cancer. However, PPARγ and its ligands exhibit a janus‐face behaviour as tumor modulators in various systems, resulting in either tumor suppression or tumor promotion. This may be in part due to signaling crosstalk to the mitogen‐activated protein kinase (MAPK) cascades. The genomic activity of PPARγ is modulated, in addition to ligand binding, by phosphorylation of a serine residue by MAPKs, such as extracellular signal‐regulated protein kinases‐1/2 (ERK‐1/2), or by nucleocytoplasmic compartmentalization through the ERK activators MAPK kinases‐1/2 (MEK‐1/2). PPARγ ligands themselves activate the ERK cascade through nongenomic and often PPARγ‐independent signaling. In the current review, we discuss the molecular mechanisms and physiological implications of the crosstalk of PPARγ with MEK‐ERK signaling and its potential as a novel drug target for cancer therapy in patients.