RRC ID |
1194
|
Author |
Yano T, Zissel G, Muller-Qernheim J, Jae Shin S, Satoh H, Ichikawa T.
|
Title |
Prostaglandin E2 reinforces the activation of Ras signal pathway in lung adenocarcinoma cells via EP3.
|
Journal |
FEBS Lett
|
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.
|
Volume |
518(1-3)
|
Pages |
154-8
|
Published |
2002-5-8
|
DOI |
10.1016/s0014-5793(02)02689-3
|
PII |
S0014579302026893
|
PMID |
11997037
|
MeSH |
Adenocarcinoma / genetics
Adenocarcinoma / metabolism*
Adenocarcinoma / pathology
Cell Division / drug effects
Cyclic AMP / biosynthesis
Dinoprostone / pharmacology*
Dose-Response Relationship, Drug
Humans
Lung Neoplasms / genetics
Lung Neoplasms / metabolism*
Lung Neoplasms / pathology
Mitogen-Activated Protein Kinase Kinases / metabolism
Mitogen-Activated Protein Kinases / metabolism
Proto-Oncogene Proteins p21(ras) / metabolism*
Pulmonary Alveoli / metabolism
Receptors, Prostaglandin E / genetics
Receptors, Prostaglandin E / metabolism*
Receptors, Prostaglandin E, EP3 Subtype
Signal Transduction
Tumor Cells, Cultured
Virulence Factors, Bordetella / pharmacology
|
IF |
3.057
|
Times Cited |
55
|
WOS Category
|
BIOPHYSICS
BIOCHEMISTRY & MOLECULAR BIOLOGY
CELL BIOLOGY
|
Resource |
Human and Animal Cells |
A549(RCB0098) |