Prostaglandin E2 reinforces the activation of Ras signal pathway in lung adenocarcinoma cells via EP3
Prostaglandin E2 reinforces the activation of Ras signal pathway in lung adenocarcinoma cells via EP3
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DOI：
10.1016/s0014-5793(02)02689-3
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发表时间：
2002-05-08
期刊：
影响因子：
3.5
通讯作者：
Ichikawa, T
中科院分区：
文献类型：
--
作者：
Yano, T;Zissel, G;Ichikawa, T
前列腺素E-2 （PGE(2)）对各种细胞反应的依赖作用受靶细胞中各自表达的PGE(2)受体（EP1、EP2、EP3、EP4）的调控。肺泡型H细胞（肺腺癌的主要祖细胞）仅表达EP4，而人肺腺癌细胞（A549）既表达EP3，也表达EP4。在A549细胞中，PGE(2)介导的Ras信号通路激活需要EP3通过调节环AATP水平对EP4产生拮抗作用。这些结果提示，EP3的表达可能是A549细胞中PGE(2)介导的Ras信号通路激活的关键因素。(C) 2002年由Elsevier Science B.V.代表欧洲生化学会联合会出版。
Prostaglandin E-2 (PGE(2))-dependent effects on various cell responses are regulated by respective PGE(2) receptors (EP1, EP2, EP3, EP4) expressing in target cells. Alveolar type H cell (a main progenitor cell of lung adenocarcinoma) expressed only EP4, while human lung adenocarcinoma cells (A549) expressed EP3 as well as EP4. An antagonistic effect of EP3 against EP4 through the modulation of cyclic AATP level is required for PGE(2)-mediated activation of Ras signal pathway in A549 cells. These results suggest that the expression of EP3 may be a critical factor for the PGE(2)-mediated activation of Ras signal pathway in A549 cells. (C) 2002 Published by Elsevier Science B.V. on behalf of the Federation of European Biochemical Societies.