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Peroxisome proliferator‐activated receptor δ as a molecular target to regulate lung cancer cell growth
Author(s) -
Fukumoto Keiko,
Yano Yoshihisa,
Virgontiga,
Hagiwara Hiromi,
Sato Hiromi,
Senba Hironobu,
Suzuki Kazuyuki,
Asano Ryuji,
Yamada Kazuhiko,
Yano Tomohiro
Publication year - 2005
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2005.06.004
Subject(s) - peroxisome proliferator activated receptor delta , agonist , biology , receptor , peroxisome proliferator activated receptor , nuclear receptor , cell growth , signal transduction , microbiology and biotechnology , cancer research , endocrinology , biochemistry , transcription factor , gene
It has been assumed that prostaglandin (PG)I 2 signaling contributes to the negative growth control of lung cancer cells; however, the mechanism remains unresolved. PGI 2 functions through a cell surface G protein‐coupled receptor (prostaglandin I2‐binding receptor, IP) and also exerts an effect by interacting with a nuclear hormone receptor, peroxisome proliferator‐activated receptor δ (PPARδ). We found that PPARδ was a key molecule of PGI 2 signaling to give negative growth control of lung cancer cells (A549), using carbarprostacyclin, a PGI 2 agonist for IP and PPARδ, and L‐165041, a PPARδ agonist. Furthermore, PPARδ‐induced cell growth control was reinforced by the inhibition of cyclooxygenase. These results suggest that PPARδ activation under the suppression of PG synthesis is important to regulate lung cancer cell growth.