Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
17
pubmed:dateCreated
2005-7-1
pubmed:abstractText
It has been assumed that prostaglandin (PG)I2 signaling contributes to the negative growth control of lung cancer cells; however, the mechanism remains unresolved. PGI2 functions through a cell surface G protein-coupled receptor (prostaglandin I2-binding receptor, IP) and also exerts an effect by interacting with a nuclear hormone receptor, peroxisome proliferator-activated receptor delta (PPARdelta). We found that PPARdelta was a key molecule of PGI2 signaling to give negative growth control of lung cancer cells (A549), using carbarprostacyclin, a PGI2 agonist for IP and PPARdelta, and L-165041, a PPARdelta agonist. Furthermore, PPARdelta-induced cell growth control was reinforced by the inhibition of cyclooxygenase. These results suggest that PPARdelta activation under the suppression of PG synthesis is important to regulate lung cancer cell growth.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0014-5793
pubmed:author
pubmed:issnType
Print
pubmed:day
4
pubmed:volume
579
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3829-36
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Peroxisome proliferator-activated receptor delta as a molecular target to regulate lung cancer cell growth.
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.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't