Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2007-10-2
pubmed:abstractText
COX-2-derived PGE2 has been implicated in the development of various types of cancers. However, the exact mechanism of PGE2-induced cancer cell proliferation and survival is still unclear. In the current study, the mechanism underlying PGE2-enhanced Erk phosphorylation in human cholangiocarcinoma cells was determined. The intracellular concentration of calcium in three cholangiocarcinoma cell lines was measured using a laser confocal scanning microscope and the expression levels of Erk and EGFR phosphorylation were determined by Western blot analyses. The activation of EP1 receptors involved in PGE2-stimulated Erk activation and increasing the intracellular concentration of calcium was elucidated using selective EP1 receptor subtype antagonists and agonist. The intracellular calcium chelator, BAPTA-AM, was shown to block PGE2-induced Erk and EGFR phosphorylation. PGE2-induced Erk phosphorylation was abrogated by pretreatment with the EGF receptor kinase inhibitor, AG1478. Our findings suggest that in human cholangiocarcinoma cells, PGE2-enhanced phosphorylation of Erk is, at least in part, mediated through EP1 receptors and EGFR phosphorylation induced by increases in the intracellular concentration of calcium.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0300-8177
pubmed:author
pubmed:issnType
Print
pubmed:volume
305
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
19-26
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Prostaglandin E2 enhances mitogen-activated protein kinase/Erk pathway in human cholangiocarcinoma cells: involvement of EP1 receptor, calcium and EGF receptors signaling.
pubmed:affiliation
Laboratory of Reproductive Medicine, Department of Pathology, Nanjing Medical University, 140 Hanzhong Road, Nanjing, Jiangsu, 210029, P.R. China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't