Abstract
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.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenocarcinoma / genetics
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Adenocarcinoma / metabolism*
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Adenocarcinoma / pathology
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Cell Division / drug effects
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Cyclic AMP / biosynthesis
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Dinoprostone / pharmacology*
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Dose-Response Relationship, Drug
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Humans
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Lung Neoplasms / genetics
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Lung Neoplasms / metabolism*
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Lung Neoplasms / pathology
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Mitogen-Activated Protein Kinase Kinases / metabolism
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Mitogen-Activated Protein Kinases / metabolism
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Proto-Oncogene Proteins p21(ras) / metabolism*
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Pulmonary Alveoli / metabolism
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Receptors, Prostaglandin E / genetics
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Receptors, Prostaglandin E / metabolism*
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Receptors, Prostaglandin E, EP3 Subtype
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Signal Transduction
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Tumor Cells, Cultured
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Virulence Factors, Bordetella / pharmacology
Substances
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PTGER3 protein, human
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Receptors, Prostaglandin E
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Receptors, Prostaglandin E, EP3 Subtype
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Virulence Factors, Bordetella
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Cyclic AMP
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Mitogen-Activated Protein Kinases
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Mitogen-Activated Protein Kinase Kinases
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HRAS protein, human
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Proto-Oncogene Proteins p21(ras)
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Dinoprostone