Linked Life Data

16328002

Source:http://linkedlifedata.com/resource/pubmed/id/16328002

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-12-5
pubmed:abstractText
The purpose of this study is to investigate the role of PI3K-Akt signaling in prostate cancer cell growth and androgen receptor (AR)-mediated gene expression. Androgen-dependent LNCaP cells and their androgen-independent counterpart, LNCaP-AI cells, were used. We found that PI3K-Akt signaling is elevated in LNCaP-AI cells compared to that in LNCaP cells and is involved in androgen-independent growth. More importantly, PI3K-Akt signaling enhances AR activity and is involved in the induction of AR target genes, such as p21(WAF/CIP), a gene with anti-apoptosis activity and associated with androgen-independent growth in human prostate cancer. A receptor tyrosine kinase inhibitor also inhibits the PI3K-Akt signaling and compromises AR activity and cell growth. These findings suggest that the PI3K-Akt cell growth survival pathway and its downstream-regulated gene, p21(WAF/CIP), are targets for developing novel therapies against prostate cancer, especially those androgen-independent diseases.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1019-6439
pubmed:author
pubmed:issnType
Print
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
245-51
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
PI3K-Akt signaling is involved in the regulation of p21(WAF/CIP) expression and androgen-independent growth in prostate cancer cells.
pubmed:affiliation
Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, OH 45267-0529, USA. shan.lu@uc.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S.