Prostaglandin E2 reinforces the activation of Ras signal pathway in lung adenocarcinoma cells via EP3

被引:57
作者
Yano, T
Zissel, G
Muller-Qernheim, J
Shin, SJ
Satoh, H
Ichikawa, T
机构
[1] Natl Inst Hlth & Nutr, Dept Food Sci Res Hlth, Shinjuku Ku, Tokyo 1628636, Japan
[2] Hosp Med, Res Ctr Borstel, D-23845 Borstel, Germany
关键词
prostaglandin E; Ras; lung adenocarcinoma; alveolar type II cell; cAMP; EP3;
D O I
10.1016/S0014-5793(02)02689-3
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:154 / 158
页数:5
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