Linked Life Data

19549589

Source:http://linkedlifedata.com/resource/pubmed/id/19549589

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2009-6-24
pubmed:abstractText
Estradiol receptor plays a key role in breast cancer and specific hormonal therapies blocking the receptor functions have been developed. Unfortunately, many patients become resistant to this treatment and develop metastatic breast tumors. The causes of breast tumor progression and hormonal therapy resistance are still debated. Many proteins are mislocalized in human cancers, and increasing evidence indicates that nuclear exclusion of estradiol receptor is involved in tumorigenesis of breast cancer cells and hormonal therapy resistance. Therefore, analysis of intracellular localization of estradiol receptor together with screening for specific compounds that redirect the mislocalized receptor to the correct subcellular compartment is a very promising approach to the discovery of novel anticancer compounds. We recently dissected estradiol receptor nuclear export in breast cancer cells and its dependence on PI3-K. This export has a strong impact on cell cycle progression. A peptide mimicking the nuclear export sequence of estradiol receptor specifically traps the receptor in nuclear compartment and blocks the S-phase entry of target cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1872-8057
pubmed:author
pubmed:issnType
Electronic
pubmed:day
24
pubmed:volume
308
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
26-31
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Signaling-dependent nuclear export of estradiol receptor controls cell cycle progression in breast cancer cells.
pubmed:affiliation
Department of General Pathology, II University of Naples, Napoli, Italy. gabriella.castoria@unina2.it
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't