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| pubmed-article:19706771 | lifeskim:mentions | umls-concept:C0376358 | lld:lifeskim |
| pubmed-article:19706771 | lifeskim:mentions | umls-concept:C0030956 | lld:lifeskim |
| pubmed-article:19706771 | lifeskim:mentions | umls-concept:C0034786 | lld:lifeskim |
| pubmed-article:19706771 | lifeskim:mentions | umls-concept:C0070099 | lld:lifeskim |
| pubmed-article:19706771 | lifeskim:mentions | umls-concept:C0033414 | lld:lifeskim |
| pubmed-article:19706771 | lifeskim:mentions | umls-concept:C1516170 | lld:lifeskim |
| pubmed-article:19706771 | lifeskim:mentions | umls-concept:C2003913 | lld:lifeskim |
| pubmed-article:19706771 | pubmed:issue | 18 | lld:pubmed |
| pubmed-article:19706771 | pubmed:dateCreated | 2009-9-16 | lld:pubmed |
| pubmed-article:19706771 | pubmed:abstractText | During progression to an androgen-independent state following androgen ablation therapy, prostate cancer cells continue to express the androgen receptor (AR) and androgen-regulated genes, indicating that AR is critical for the proliferation of hormone-refractory prostate cancer cells. Multiple mechanisms have been proposed for the development of AR-dependent hormone-refractory disease, including changes in expression of AR coregulatory proteins, AR mutation, growth factor-mediated activation of AR, and AR protein up-regulation. The most prominent of these progressive changes is the up-regulation of AR that occurs in >90% of prostate cancers. A common feature of the most aggressive hormone-refractory prostate cancers is the accumulation of cells with neuroendocrine characteristics that produce paracrine factors and may provide a novel mechanism for the regulation of AR during advanced stages of the disease. In this study, we show that neuroendocrine-derived parathyroid hormone-related protein (PTHrP)-mediated signaling through the epidermal growth factor receptor (EGFR) and Src pathways contributes to the phenotype of advanced prostate cancer by reducing AR protein turnover. PTHrP-induced accumulation of AR depended on the activity of Src and EGFR and consequent phosphorylation of the AR on Tyr(534). PTHrP-induced tyrosine phosphorylation of AR resulted in reduced AR ubiquitination and interaction with the ubiquitin ligase COOH terminus of Hsp70-interacting protein. These events result in increased accumulation of AR and thus enhanced growth of prostate cancer cells at low levels of androgen. | lld:pubmed |
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| pubmed-article:19706771 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:19706771 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:19706771 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19706771 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:19706771 | pubmed:issn | 1538-7445 | lld:pubmed |
| pubmed-article:19706771 | pubmed:author | pubmed-author:WeberMichael... | lld:pubmed |
| pubmed-article:19706771 | pubmed:author | pubmed-author:ParsonsSarah... | lld:pubmed |
| pubmed-article:19706771 | pubmed:author | pubmed-author:GioeliDanielD | lld:pubmed |
| pubmed-article:19706771 | pubmed:author | pubmed-author:DaSilvaJohnJ | lld:pubmed |
| pubmed-article:19706771 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19706771 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:19706771 | pubmed:volume | 69 | lld:pubmed |
| pubmed-article:19706771 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19706771 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19706771 | pubmed:pagination | 7402-11 | lld:pubmed |
| pubmed-article:19706771 | pubmed:dateRevised | 2011-9-26 | lld:pubmed |
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| pubmed-article:19706771 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19706771 | pubmed:articleTitle | The neuroendocrine-derived peptide parathyroid hormone-related protein promotes prostate cancer cell growth by stabilizing the androgen receptor. | lld:pubmed |
| pubmed-article:19706771 | pubmed:affiliation | Department of Microbiology and Cancer Center, University of Virginia Health System, Charlottesville, Virginia 22908-0734, USA. | lld:pubmed |
| pubmed-article:19706771 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19706771 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:19706771 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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