Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-3
pubmed:dateCreated
2002-5-8
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0014-5793
pubmed:author
pubmed:issnType
Print
pubmed:day
8
pubmed:volume
518
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
154-8
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:11997037-Adenocarcinoma, pubmed-meshheading:11997037-Cell Division, pubmed-meshheading:11997037-Cyclic AMP, pubmed-meshheading:11997037-Dinoprostone, pubmed-meshheading:11997037-Dose-Response Relationship, Drug, pubmed-meshheading:11997037-Humans, pubmed-meshheading:11997037-Lung Neoplasms, pubmed-meshheading:11997037-Mitogen-Activated Protein Kinase Kinases, pubmed-meshheading:11997037-Mitogen-Activated Protein Kinases, pubmed-meshheading:11997037-Proto-Oncogene Proteins p21(ras), pubmed-meshheading:11997037-Pulmonary Alveoli, pubmed-meshheading:11997037-Receptors, Prostaglandin E, pubmed-meshheading:11997037-Receptors, Prostaglandin E, EP3 Subtype, pubmed-meshheading:11997037-Signal Transduction, pubmed-meshheading:11997037-Tumor Cells, Cultured, pubmed-meshheading:11997037-Virulence Factors, Bordetella
pubmed:year
2002
pubmed:articleTitle
Prostaglandin E2 reinforces the activation of Ras signal pathway in lung adenocarcinoma cells via EP3.
pubmed:affiliation
Department of Food Science Research for Health, National Institute of Health and Nutrition, 1-23-1 Toyama, Shinjuku-ku, Tokyo 162-8636, Japan. yano@nih.go.jp
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't