Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
18
pubmed:dateCreated
2000-10-5
pubmed:abstractText
In the prostate gland of adult mammals, most epithelial cells are in a state of proliferative quiescence. Androgens regulate this effect by inducing cell cycle arrest in the G(0)/G(1) phase. Potential mediators of this androgen-induced proliferative shutoff were identified by means of subtracted cDNA libraries. The expression pattern of one of these sequences, AS3, strongly correlated with the expression of the androgen-induced proliferative shutoff both temporally and dosewise. The AS3 gene is located on chromosome 13 q12.3, in close proximity to the BRCA2 gene. The loss of chromosomal regions where AS3 alleles are located correlates with various human cancers, including prostate. The biological effect of AS3 was tested in two stable cell lines, one expressing sense and another expressing antisense AS3 constructs, both under tetracycline regulation. S9 cells were obtained by retroviral infection with virions containing a tetracycline-regulated sense AS3 construct. In these cells, sense AS3 was negatively regulated by tetracycline. Tetracycline withdrawal increased the expression of AS3 mRNA and protein. The expression of tetracycline-regulated AS3 resulted in inhibition of cell proliferation. A4 cells were obtained by retroviral infection with virions containing a tetracycline-regulated antisense AS3 construct. Vector-driven expression of antisense-AS3 blocked the induction of androgen-induced endogenous AS3 mRNA and blocked the inhibitory effect of androgens on cell proliferation. Tetracycline-regulated expression of the empty vector control had no effect on cell proliferation. These experiments strongly suggest that AS3 is a mediator of the androgen-induced proliferative shutoff.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/10963680-10215036, http://linkedlifedata.com/resource/pubmed/commentcorrection/10963680-10231032, http://linkedlifedata.com/resource/pubmed/commentcorrection/10963680-10428037, http://linkedlifedata.com/resource/pubmed/commentcorrection/10963680-13437312, http://linkedlifedata.com/resource/pubmed/commentcorrection/10963680-15433723, http://linkedlifedata.com/resource/pubmed/commentcorrection/10963680-1722336, http://linkedlifedata.com/resource/pubmed/commentcorrection/10963680-180681, http://linkedlifedata.com/resource/pubmed/commentcorrection/10963680-1958538, http://linkedlifedata.com/resource/pubmed/commentcorrection/10963680-2260966, http://linkedlifedata.com/resource/pubmed/commentcorrection/10963680-2731169, http://linkedlifedata.com/resource/pubmed/commentcorrection/10963680-4168724, http://linkedlifedata.com/resource/pubmed/commentcorrection/10963680-6831420, http://linkedlifedata.com/resource/pubmed/commentcorrection/10963680-7277602, http://linkedlifedata.com/resource/pubmed/commentcorrection/10963680-7511045, http://linkedlifedata.com/resource/pubmed/commentcorrection/10963680-7577475, http://linkedlifedata.com/resource/pubmed/commentcorrection/10963680-7585515, http://linkedlifedata.com/resource/pubmed/commentcorrection/10963680-8375649, http://linkedlifedata.com/resource/pubmed/commentcorrection/10963680-8781411, http://linkedlifedata.com/resource/pubmed/commentcorrection/10963680-8866667, http://linkedlifedata.com/resource/pubmed/commentcorrection/10963680-8876218, http://linkedlifedata.com/resource/pubmed/commentcorrection/10963680-9075695, http://linkedlifedata.com/resource/pubmed/commentcorrection/10963680-9459187, http://linkedlifedata.com/resource/pubmed/commentcorrection/10963680-9658399, http://linkedlifedata.com/resource/pubmed/commentcorrection/10963680-9734811
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0027-8424
pubmed:author
pubmed:issnType
Print
pubmed:day
29
pubmed:volume
97
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
10185-90
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed-meshheading:10963680-Amino Acid Sequence, pubmed-meshheading:10963680-Androgens, pubmed-meshheading:10963680-Cell Nucleus, pubmed-meshheading:10963680-Chromosome Mapping, pubmed-meshheading:10963680-Chromosomes, Human, Pair 13, pubmed-meshheading:10963680-DNA, Antisense, pubmed-meshheading:10963680-DNA, Complementary, pubmed-meshheading:10963680-DNA-Binding Proteins, pubmed-meshheading:10963680-Gene Expression Regulation, Neoplastic, pubmed-meshheading:10963680-Gene Library, pubmed-meshheading:10963680-Humans, pubmed-meshheading:10963680-Male, pubmed-meshheading:10963680-Molecular Sequence Data, pubmed-meshheading:10963680-Neoplasm Proteins, pubmed-meshheading:10963680-Prostatic Neoplasms, pubmed-meshheading:10963680-Repressor Proteins, pubmed-meshheading:10963680-Tetracycline, pubmed-meshheading:10963680-Trans-Activators, pubmed-meshheading:10963680-Transcription, Genetic, pubmed-meshheading:10963680-Transcription Factors, pubmed-meshheading:10963680-Transfection, pubmed-meshheading:10963680-Tumor Cells, Cultured
pubmed:year
2000
pubmed:articleTitle
Androgen-induced proliferative quiescence in prostate cancer cells: the role of AS3 as its mediator.
pubmed:affiliation
Department of Anatomy and Cell Biology, Tufts University School of Medicine, 136 Harrison Avenue, Boston, MA 02111, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't