Linked Life Data

16964290

Source:http://linkedlifedata.com/resource/pubmed/id/16964290

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2007-3-8
pubmed:abstractText
The growth and progression of prostate cancer are dependent on androgens and androgen receptor (AR), which act by modulating gene expression. Utilizing a gene microarray approach, we have identified the alpha1-subunit gene of soluble guanylyl cyclase (sGC) as a novel androgen-regulated gene. A heterodimeric cytoplasmic protein composed of one alpha and one beta subunit, sGC mediates the widespread cellular effects of nitric oxide (NO). We report here that, in prostate cancer cells, androgens stimulate the expression of sGCalpha1. A cloned human sGCalpha1 promoter is activated by androgen in an AR-dependent manner, suggesting that sGCalpha1 may be a direct AR target gene. Disruption of sGCalpha1 expression severely compromises the growth of both androgen-dependent and androgen-independent AR-positive prostate cancer cells. Overexpression of sGCalpha1 alone is sufficient for stimulating prostate cancer cell proliferation. Interestingly, the major growth effect of sGCalpha1 is independent of NO and cyclic guanosine monophosphate, a major mediator of the sGC enzyme. These data strongly suggest that sGCalpha1 acts in prostate cancer via a novel pathway that does not depend on sGCbeta1. Tissue studies show that sGCalpha1 expression is significantly elevated in advanced prostate cancer. Thus, sGCalpha1 may be an important mediator of the procarcinogenic effects of androgens.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:day
8
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1606-15
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Androgen regulation of soluble guanylyl cyclasealpha1 mediates prostate cancer cell proliferation.
pubmed:affiliation
Department of Biological Sciences, University of Toledo, Toledo, OH 43606, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural