Linked Life Data

19245796

Source:http://linkedlifedata.com/resource/pubmed/id/19245796

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2009-3-30
pubmed:abstractText
The epithelial-mesenchymal transition (EMT), a crucial event in cancer progression and embryonic development, is induced by transforming growth factor (TGF)-beta. Expression of E-cadherin, a representative epithelial marker, is repressed through transcriptional reduction by TGF-beta. Here, we show that endocytosis of cell surface E-cadherin during EMT induced by TGF-beta and during scattering induced by hepatocyte growth factor (HGF) can be blocked by inhibiting proteasome with lactacystin and MG132 in normal epithelial cells and in cancer cells. Although loss of cell surface E-cadherin following TGF-beta treatment induced translocation of beta-catenin, an E-cadherin-anchoring molecule, to the nucleus, proteasome inhibition prevented this process and resulted in co-localization of beta-catenin with E-cadherin at the cell surface, leading to establishment of cell-cell adhesion. However, promotion of cell migration by TGF-beta was not significantly affected by proteasome inhibition. Proteasome-dependent events thus appear to be involved in stabilization of cell surface E-cadherin.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1090-2104
pubmed:author
pubmed:issnType
Electronic
pubmed:day
17
pubmed:volume
381
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
560-5
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Regulation of the stability of cell surface E-cadherin by the proteasome.
pubmed:affiliation
Department of Molecular Pathology, University of Tokyo, Bunkyo-ku, Japan. msaitoh-ind@umin.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't