Linked Life Data

20971111

Source:http://linkedlifedata.com/resource/pubmed/id/20971111

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
22
pubmed:dateCreated
2010-11-15
pubmed:abstractText
Epithelial-to-mesenchymal transition (EMT) has been implicated in various physiological and pathological events. In this study, we found that the synthetic glucocorticoid dexamethasone (Dex) can inhibit transforming growth factor-beta1-induced EMT and cell migration. We also demonstrated that Dex inhibits EMT through a mechanism involving the suppression of ROS generation. Surprisingly, Dex alone induced mesenchymal-to-epithelial transition (MET). Dexamethasone treatment abolished Snail1 binding to the E-cadherin promoter, suggesting that suppression of Snail1 contributes to the above roles of Dex. Our findings demonstrate that Dex functions as both a suppressor of EMT and as an inducer of MET and therefore may be implicated in certain pathophysiological events.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1873-3468
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
19
pubmed:volume
584
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4646-54
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Glucocorticoid induces mesenchymal-to-epithelial transition and inhibits TGF-?1-induced epithelial-to-mesenchymal transition and cell migration.
pubmed:affiliation
Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences. 320 Yue-Yang Road, Shanghai 200031, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't