Linked Life Data

17085387

Source:http://linkedlifedata.com/resource/pubmed/id/17085387

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2006-11-6
pubmed:abstractText
We investigated the effect of constitutive active Akt expression on anti-proliferative and apoptotic effect of tamoxifen in MCF-7 human breast cancer cells. Forced expression of AktDD (T308D, S473D) resulted in increased phosphorylation of GSK3beta, a physiological substrate of Akt. When estrogen receptor (ER) mediated transcription was determined by luciferase assays, there was more than 2-fold increase in estradiol-dependent transcription in MCF-7 cells overexpressing AktDD (MCF-7 AktDD) compared to vector control cells (MCF-7 vec). MCF-7 AktDD cells showed increased proliferation in a medium containing charcoal stripped serum supplemented with estradiol. When the cell cycle profiles were examined, there was an increase in S-phase and a reduction in G1 phase in MCF-7 AktDD cells as compared to MCF-7 vec cells. Overexpression of AktDD also attenuated tamoxifen-mediated apoptosis. These results suggest that Akt could confer resistance to anti-estrogen mediated cell death and inhibition of proliferation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1521-6543
pubmed:author
pubmed:issnType
Print
pubmed:volume
58
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
664-9
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Expression of active Akt protects against tamoxifen-induced apoptosis in MCF-7 Cells.
pubmed:affiliation
Department of Cancer Biology, Vanderbilt-Ingram Comprehensive Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-6307, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural