Linked Life Data

11389065

Source:http://linkedlifedata.com/resource/pubmed/id/11389065

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2001-6-4
pubmed:abstractText
Previously, we demonstrated that up-regulation of caveolin-1 (cav-1) was associated with prostate cancer metastasis, biochemical recurrence after radical prostatectomy, and androgen insensitivity. The objective of this study was to characterize the regulation of cav-1 by testosterone (T) and to test the effects of cav-1 on prostate cancer cell survival/clonal growth and metastatic activities. Our results demonstrated that T up-regulated cav-1 protein levels in part through transcriptional regulation and significantly enhanced survival of prostate cancer cell lines ABAC3 and LNCaP after serum starvation (>40% and >60% increased viability, respectively) and in an extended clonogenic assay (approximately 4-fold and 6-fold increase in colonies, respectively). Importantly, antisense cav-1 inhibited the survival effects of T in these assay systems. Modest but not high levels of adenoviral vector-mediated cav-1 expression alone also significantly increased viability (>40%) and clonal growth (10-fold increase in colonies) after serum starvation. Analysis of spontaneous metastasis in stably transfected antisense cav-1 mouse prostate cancer cell clones demonstrated reduction of spontaneous lymph node metastasis incidence (13%), spontaneous lymph node metastasis volume (46%), and experimental lung metastasis incidence (40%) compared with vector control cell clones. Surgical castration further reduced spontaneous lymph node metastasis incidence and volume (18% and 28%, respectively) in antisense cancer cell clones, but not in vector control clones. Our studies demonstrate that cav-1 is a downstream effector of T-mediated prostate cancer cell survival/clonal growth and that modest levels of cav-1 can independently promote prostate cancer cell survival/clonal growth and metastatic activities.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
61
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4386-92
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:11389065-Animals, pubmed-meshheading:11389065-Caveolin 1, pubmed-meshheading:11389065-Caveolins, pubmed-meshheading:11389065-Cell Division, pubmed-meshheading:11389065-Cell Survival, pubmed-meshheading:11389065-DNA, Antisense, pubmed-meshheading:11389065-Dose-Response Relationship, Drug, pubmed-meshheading:11389065-Humans, pubmed-meshheading:11389065-Lung Neoplasms, pubmed-meshheading:11389065-Lymphatic Metastasis, pubmed-meshheading:11389065-Male, pubmed-meshheading:11389065-Mice, pubmed-meshheading:11389065-Neoplasm Metastasis, pubmed-meshheading:11389065-Neoplasms, Hormone-Dependent, pubmed-meshheading:11389065-Promoter Regions, Genetic, pubmed-meshheading:11389065-Prostatic Neoplasms, pubmed-meshheading:11389065-Testosterone, pubmed-meshheading:11389065-Transcriptional Activation, pubmed-meshheading:11389065-Tumor Cells, Cultured, pubmed-meshheading:11389065-Up-Regulation
pubmed:year
2001
pubmed:articleTitle
Caveolin-1 mediates testosterone-stimulated survival/clonal growth and promotes metastatic activities in prostate cancer cells.
pubmed:affiliation
Scott Department of Urology, Baylor College of Medicine, 6560 Fannon, Houston, TX 77030, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.