Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
24
pubmed:dateCreated
2003-12-25
pubmed:abstractText
The constitutive activation of signal transducer and activator of transcription (STAT) proteins has been demonstrated in many diverse human cancer cell lines and clinical tumors including prostate cancer. The STAT family has at least seven members, and the two forms of the STAT5 protein, STAT5A and STAT5B, exhibit a high degree of sequence similarity. We have reported previously that expression of STAT5B, but not STAT5A, could enhance the transforming potential of v-src and induces cell cycle progression and motility in fibroblasts. In the current study we demonstrate specific activation of STAT5B in epithelial cells representing invasive and metastatic prostate cancer. We also demonstrate that the naturally occurring dominant-negative isoform STAT5DeltaB can block cell cycle progression through G(1) and inhibit the growth, invasive potential, and clonogenic ability of these prostate cancer cell lines. Furthermore, we report that the dominant-negative isoform STAT5DeltaB can inhibit the growth of prostate cancer cells in grafting studies. These results support our hypothesis that specific activation of STAT5, in particular STAT5B, facilitates the progression of prostate cancer.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
63
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
8757-62
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Activation of signal transducer and activator of transcription 5 is required for progression of autochthonous prostate cancer: evidence from the transgenic adenocarcinoma of the mouse prostate system.
pubmed:affiliation
Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.