Linked Life Data

20606309

Source:http://linkedlifedata.com/resource/pubmed/id/20606309

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2010-7-7
pubmed:abstractText
Lung cancer is a leading cause of morbidity and mortality worldwide. Cyclooxygenase-2 (COX-2) expression is upregulated in lung carcinomas and is considered an attractive therapeutic target. In this study, the effect of curcumin and curcumin analogues on COX-2 expression induced by phorbol 12-myristate 13-acetate (PMA) were investigated. We found that a novel curcumin analogue (GL63) inhibited PMA-induced COX-2 mRNA and protein levels in H460 cells to a greater degree than curcumin. To understand the molecular mechanisms governing COX-2 regulation, the effect on COX-2 mRNA degradation was examined; we found that GL63 significantly decreased COX-2 mRNA stability by reducing cytoplasmic localization and protein abundance of human antigen R (HuR). The 3'-untranslated region (3'-UTR) report gene assay also showed GL63 substantially reduced the 3'-UTR green fluorescent protein values, indicating that the destabilizing effect on COX-2 mRNA may be couple with the posttranscriptional inhibition of COX-2. Taken together, our results provide evidence that the novel curcumin analogue can effectively inhibit PMA-induced COX-2 expression in H460 cells, a mechanism associated with COX-2 mRNA stability and post-transcriptional regulation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1347-5215
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
33
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1170-5
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
A new cyclooxygenase-2 inhibitor, (1E,4E)-1,5-bis(2-bromophenyl)penta-1,4-dien-3-one (GL63) suppresses cyclooxygenase-2 gene expression in human lung epithelial cancer cells: coupled mRNA stabilization and posttranscriptional inhibition.
pubmed:affiliation
Department of Pathophysiology, Sun Yat-Sen University, Guangzhou 510080, P. R. China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't