Peroxisome proliferator-activated receptor δ as a molecular target to regulate lung cancer cell growth
Peroxisome proliferator-activated receptor δ as a molecular target to regulate lung cancer cell growth
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作为调控肺癌细胞生长分子靶点的过氧化物酶体增殖激活受体δ
DOI：
10.1016/j.febslet.2005.06.004
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发表时间：
2005-07-04
期刊：
影响因子：
3.5
通讯作者：
Yano, T
中科院分区：
文献类型：
--
作者：
Fukumoto, K;Yano, Y;Yano, T
据推测，前列腺素（PG）12信号有助于肺癌细胞的负生长控制;然而，其机制尚未解决。PGI（2）通过细胞表面G蛋白偶联受体（前列腺素I2结合受体，IP）发挥作用，也通过与核激素受体过氧化物酶体增殖物激活受体δ（过氧化物酶体增殖物激活受体δ）相互作用发挥作用。我们发现，PPARdelta是PGI（2）信号传导的关键分子，使用卡巴前列环素（一种IP和PPARdelta的PGI（2）激动剂）和L-165041（一种PPARdelta激动剂）对肺癌细胞（A549）进行负生长控制。此外，通过抑制环氧合酶，增强了PPAR δ诱导的细胞生长控制。这些结果表明，在PG合成的抑制下，PPAR δ的激活对调节肺癌细胞生长是重要的。(c)2005年欧洲生物化学学会联合会。Elsevier B. V.出版，保留所有权利。
It has been assumed that prostaglandin (PG)12 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 delta (PPAR delta). We found that PPAR delta 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 PPAR delta, and L-165041, a PPAR delta agonist. Furthermore, PPAR delta-induced cell growth control was reinforced by the inhibition of cyclooxygenase. These results suggest that PPAR delta activation under the suppression of PG synthesis is important to regulate lung cancer cell growth. (c) 2005 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.