Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
33
pubmed:dateCreated
2002-7-25
pubmed:abstractText
To gain insight into the molecular basis of human prolactin (hPRL) antagonist induced apoptosis, we compared the differential gene expression profile of four human breast cancer cell lines following treatment with hPRL and its antagonist (hPRL-G129R). Among the genes identified, the bcl-2 gene was of particular interest. We found that bcl-2 mRNA was up regulated in three of the four cell lines that were treated with hPRL. To further confirm these results, real time RT-PCR and ELISA analyses were used to detect bcl-2 mRNA and Bcl-2 protein, respectively, in 11 different breast cancer cell lines after hPRL or hPRL-G129R treatment. Our data suggests that Bcl-2 is up-regulated in response to hPRL stimulation and is competitively inhibited by hPRL-G129R in the majority of the cell lines tested. Thus, we propose that the anti-apoptotic role of hPRL in breast cancer is mediated, at least in part, through regulation of Bcl-2.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5047-55
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Regulation of bcl-2 gene expression in human breast cancer cells by prolactin and its antagonist, hPRL-G129R.
pubmed:affiliation
Department of Microbiology and Molecular Medicine, Clemson University, Clemson, South Carolina, SC 29630, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't