PMID- 18528526
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20110714
LR  - 20220224
IS  - 1687-4757 (Print)
IS  - 1687-4765 (Electronic)
VI  - 2008
DP  - 2008
TI  - Synergistic Effects of PPARgamma Ligands and Retinoids in Cancer Treatment.
PG  - 181047
LID - 10.1155/2008/181047 [doi]
LID - 181047
AB  - Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear 
      receptor superfamily. The activation of PPARs by their specific ligands is 
      regarded as one of the promising strategies to inhibit cancer cell growth. 
      However, recent clinical trials targeting several common cancers showed no 
      beneficial effect when PPAR ligands are used as a monotherapy. Retinoid X 
      receptors (RXRs), which play a critical role in normal cell proliferation as a 
      master regulator for nuclear receptors, preferentially form heterodimers with 
      PPARs. A malfunction of RXRalpha due to phosphorylation by the Ras/MAPK signaling 
      pathway is associated with the development of certain types of human 
      malignancies. The activation of PPARgamma/RXR heterodimer by their respective 
      ligands synergistically inhibits cell growth, while inducing apoptosis in human 
      colon cancer cells when the phosphorylation of RXRalpha was inhibited. We herein 
      review the synergistic antitumor effects produced by the combination of the PPAR, 
      especially PPARgamma, ligands plus other agents, especially retinoids, in a 
      variety of human cancers. We also focus on the phosphorylation of RXRalpha 
      because the inhibition of RXRalpha phosphorylation and the restoration of its 
      physiological function may activate PPAR/RXR heterodimer and, therefore, be a 
      potentially effective and critical strategy for the inhibition of cancer cell 
      growth.
FAU - Shimizu, Masahito
AU  - Shimizu M
AD  - Department of Medicine, Gifu University Graduate School of Medicine, Gifu 
      501-1194, Japan.
FAU - Moriwaki, Hisataka
AU  - Moriwaki H
LA  - eng
PT  - Journal Article
PL  - United States
TA  - PPAR Res
JT  - PPAR research
JID - 101269101
PMC - PMC2408709
EDAT- 2008/06/06 09:00
MHDA- 2008/06/06 09:01
PMCR- 2008/05/28
CRDT- 2008/06/06 09:00
PHST- 2008/02/26 00:00 [received]
PHST- 2008/04/21 00:00 [revised]
PHST- 2008/05/01 00:00 [accepted]
PHST- 2008/06/06 09:00 [pubmed]
PHST- 2008/06/06 09:01 [medline]
PHST- 2008/06/06 09:00 [entrez]
PHST- 2008/05/28 00:00 [pmc-release]
AID - 10.1155/2008/181047 [doi]
PST - ppublish
SO  - PPAR Res. 2008;2008:181047. doi: 10.1155/2008/181047.