| pubmed-article:11389065 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11389065 | lifeskim:mentions | umls-concept:C0376358 | lld:lifeskim |
| pubmed-article:11389065 | lifeskim:mentions | umls-concept:C0379710 | lld:lifeskim |
| pubmed-article:11389065 | lifeskim:mentions | umls-concept:C1704387 | lld:lifeskim |
| pubmed-article:11389065 | lifeskim:mentions | umls-concept:C1522642 | lld:lifeskim |
| pubmed-article:11389065 | lifeskim:mentions | umls-concept:C0334227 | lld:lifeskim |
| pubmed-article:11389065 | lifeskim:mentions | umls-concept:C1522484 | lld:lifeskim |
| pubmed-article:11389065 | lifeskim:mentions | umls-concept:C0038952 | lld:lifeskim |
| pubmed-article:11389065 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:11389065 | lifeskim:mentions | umls-concept:C0033414 | lld:lifeskim |
| pubmed-article:11389065 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
| pubmed-article:11389065 | lifeskim:mentions | umls-concept:C0036525 | lld:lifeskim |
| pubmed-article:11389065 | lifeskim:mentions | umls-concept:C0086597 | lld:lifeskim |
| pubmed-article:11389065 | pubmed:issue | 11 | lld:pubmed |
| pubmed-article:11389065 | pubmed:dateCreated | 2001-6-4 | lld:pubmed |
| pubmed-article:11389065 | 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. | lld:pubmed |
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| pubmed-article:11389065 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11389065 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11389065 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11389065 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11389065 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:11389065 | pubmed:issn | 0008-5472 | lld:pubmed |
| pubmed-article:11389065 | pubmed:author | pubmed-author:WangJJ | lld:pubmed |
| pubmed-article:11389065 | pubmed:author | pubmed-author:SatohTT | lld:pubmed |
| pubmed-article:11389065 | pubmed:author | pubmed-author:LORR | lld:pubmed |
| pubmed-article:11389065 | pubmed:author | pubmed-author:NashDD | lld:pubmed |
| pubmed-article:11389065 | pubmed:author | pubmed-author:YanoOO | lld:pubmed |
| pubmed-article:11389065 | pubmed:author | pubmed-author:EbaraSS | lld:pubmed |
| pubmed-article:11389065 | pubmed:author | pubmed-author:ThompsonT CTC | lld:pubmed |
| pubmed-article:11389065 | pubmed:author | pubmed-author:TimmeT LTL | lld:pubmed |
| pubmed-article:11389065 | pubmed:author | pubmed-author:RehMM | lld:pubmed |
| pubmed-article:11389065 | pubmed:author | pubmed-author:TahirS ASA | lld:pubmed |
| pubmed-article:11389065 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11389065 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:11389065 | pubmed:volume | 61 | lld:pubmed |
| pubmed-article:11389065 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11389065 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11389065 | pubmed:pagination | 4386-92 | lld:pubmed |
| pubmed-article:11389065 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:11389065 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11389065 | pubmed:articleTitle | Caveolin-1 mediates testosterone-stimulated survival/clonal growth and promotes metastatic activities in prostate cancer cells. | lld:pubmed |
| pubmed-article:11389065 | pubmed:affiliation | Scott Department of Urology, Baylor College of Medicine, 6560 Fannon, Houston, TX 77030, USA. | lld:pubmed |
| pubmed-article:11389065 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11389065 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:11389065 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
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