Linked Life Data

16455820

Source:http://linkedlifedata.com/resource/pubmed/id/16455820

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2006-5-2
pubmed:abstractText
The basic leucine zipper transcription factor, CCAAT enhancer-binding protein-alpha (C/EBPalpha), negatively regulates cell proliferation and induces terminal differentiation of various cell types. C/EBPalpha is expressed in the prostate, but its potential role in the tissue is unknown. Herein, we show that C/EBPalpha is highly expressed at the stage of growth arrest during prostate development. Furthermore, overexpression of C/EBPalpha decreases the rate of DNA synthesis in LNCaP prostate cancer cells. Investigation of the potential cross-talk between C/EBPalpha and androgen receptor (AR) that is responsible for androgen-dependent prostate proliferation demonstrates that androgen-dependent transactivation of AR is strongly repressed by C/EBPalpha. C/EBPalpha directly binds AR in vitro and forms a complex with AR in vivo. C/EBPalpha neither prevents the nuclear translocation of AR nor disrupts the N/C-terminal interaction of AR, which are both necessary for its proper transactivation activity upon ligand binding. To modulate AR transactivation, however, C/EBPalpha does compete with AR coactivators for AR binding. Additionally, C/EBPalpha is recruited onto AR-target promoters with AR and is further able to inhibit the expression of endogenous prostate-specific antigen in prostate cancer cells. Our results suggest C/EBPalpha as a potent AR corepressor and provide insight into the role of C/EBPalpha in prostate development and cancer.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0888-8809
pubmed:author
pubmed:issnType
Print
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
984-95
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:16455820-Androgen Receptor Antagonists, pubmed-meshheading:16455820-Animals, pubmed-meshheading:16455820-CCAAT-Enhancer-Binding Protein-alpha, pubmed-meshheading:16455820-Cell Line, Tumor, pubmed-meshheading:16455820-Cell Proliferation, pubmed-meshheading:16455820-Down-Regulation, pubmed-meshheading:16455820-Gene Expression Regulation, Neoplastic, pubmed-meshheading:16455820-Humans, pubmed-meshheading:16455820-Male, pubmed-meshheading:16455820-Promoter Regions, Genetic, pubmed-meshheading:16455820-Prostate, pubmed-meshheading:16455820-Prostate-Specific Antigen, pubmed-meshheading:16455820-Prostatic Neoplasms, pubmed-meshheading:16455820-Rats, pubmed-meshheading:16455820-Receptors, Androgen, pubmed-meshheading:16455820-Repressor Proteins, pubmed-meshheading:16455820-Transcriptional Activation
pubmed:year
2006
pubmed:articleTitle
The CCAAT enhancer-binding protein-alpha negatively regulates the transactivation of androgen receptor in prostate cancer cells.
pubmed:affiliation
Hormone Research Center, School of Biological Sciences and Technology, Chonnam National University, Gwangju 500-757, Republic of Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't