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

FEBS Letters

Muller-Qernheim, Joachim²  Ichikawa, Tomio³  Satoh, Haruna¹  Jae Shin, Sung¹  Yano, Tomohiro¹  Zissel, Gernot² 

[1] Department of Food Science Research for Health, National Institute of Health and Nutrition, 1-23-1 Toyama, Shinjuku-ku, Tokyo 162-8636, Japan;Research Centre Borstel, Medical Hospital, 23845 Borstel, Germany;Department of Life Environmental Science, Mukogawa Womens’ College, Hyogo 663-8558, Japan

关键词: Prostaglandin E2;    Ras;    Lung adenocarcinoma;    Alveolar type II cell;    cAMP;    EP3;    cAMP;    cyclic AMP;    NSCLC;    non-small cell lung cancer;    PGE2;    prostaglandin E2;    COX-2;    cyclooxygenase-2;    FCS;    fetal calf serum;    PTX;    pertussis toxin;    IBMX;    isobutylmethylxanthine;    Erk;    extracellular signal-regulated kinase;    Mek-P;    phosphorylated Mek;    Erk-P;    phosphorylated Erk;    G protein;    heterotrimeric guanine nucleotide-binding regulatory protein;    AC;    adenylate cyclase;    PKA;    protein kinase A;   

DOI  :  10.1016/S0014-5793(02)02689-3

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Prostaglandin E₂ (PGE₂)-dependent effects on various cell responses are regulated by respective PGE₂ receptors (EP₁, EP₂, EP₃, EP₄) expressing in target cells. Alveolar type II 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 AMP level is required for PGE₂-mediated activation of Ras signal pathway in A549 cells. These results suggest that the expression of EP₃ may be a critical factor for the PGE₂-mediated activation of Ras signal pathway in A549 cells.

【 授权许可】

Unknown