pubmed-article:1309535 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1309535 | lifeskim:mentions | umls-concept:C0600139 | lld:lifeskim |
pubmed-article:1309535 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
pubmed-article:1309535 | lifeskim:mentions | umls-concept:C1518174 | lld:lifeskim |
pubmed-article:1309535 | lifeskim:mentions | umls-concept:C0243192 | lld:lifeskim |
pubmed-article:1309535 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
pubmed-article:1309535 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:1309535 | pubmed:dateCreated | 1992-2-10 | lld:pubmed |
pubmed-article:1309535 | pubmed:abstractText | To develop a new approach to the treatment of advanced, hormone-refractory prostate cancer, the signal transductions regulating the growth of human androgen-independent prostate carcinoma cell lines were studied. Agonist-stimulated Ca2+ mobilization, a critical regulatory event in other secretory cell types, was studied as a means of identifying previously undescribed plasma membrane receptors that may transduce a growth inhibitory signal. In all of the cell lines tested, P2-purinergic receptor agonists, including ATP and certain hydrolysis-resistant adenine nucleotides, induced a rapid, transient increase in cytoplasmic free Ca2+ that was detectable at 50 to 100 nM ATP, was maximal at 100 microM ATP, and was inhibited approximately 50% by chelation of extracellular Ca2+. Within 8 s after addition, ATP stimulated accumulation of the polyphosphatidylinositol products inositol (1, 4, 5) trisphosphate, inositol (1, 3, 4) trisphosphate, and inositol tetrakisphosphate. In addition to stimulating phosphatidylinositol turnover and Ca2+ mobilization, ATP and hydrolysis-resistant ATP analogues induced greater than 90% inhibition of the growth of all lines tested. These data demonstrate that human androgen-independent prostate carcinoma cells express functional P2-purinergic receptors linked to phospholipase C, and that agonists of this receptor are markedly growth inhibitory, suggesting a novel therapeutic approach to this common adult neoplasm. | lld:pubmed |
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pubmed-article:1309535 | pubmed:language | eng | lld:pubmed |
pubmed-article:1309535 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1309535 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:1309535 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1309535 | pubmed:month | Jan | lld:pubmed |
pubmed-article:1309535 | pubmed:issn | 0021-9738 | lld:pubmed |
pubmed-article:1309535 | pubmed:author | pubmed-author:MyersC ECE | lld:pubmed |
pubmed-article:1309535 | pubmed:author | pubmed-author:TrepelJ BJB | lld:pubmed |
pubmed-article:1309535 | pubmed:author | pubmed-author:CaseF HFH3rd | lld:pubmed |
pubmed-article:1309535 | pubmed:author | pubmed-author:FangW GWG | lld:pubmed |
pubmed-article:1309535 | pubmed:author | pubmed-author:PirniaFF | lld:pubmed |
pubmed-article:1309535 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1309535 | pubmed:volume | 89 | lld:pubmed |
pubmed-article:1309535 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1309535 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1309535 | pubmed:pagination | 191-6 | lld:pubmed |
pubmed-article:1309535 | pubmed:dateRevised | 2010-9-7 | lld:pubmed |
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pubmed-article:1309535 | pubmed:year | 1992 | lld:pubmed |
pubmed-article:1309535 | pubmed:articleTitle | P2-purinergic receptor agonists inhibit the growth of androgen-independent prostate carcinoma cells. | lld:pubmed |
pubmed-article:1309535 | pubmed:affiliation | Clinical Pharmacology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. | lld:pubmed |
pubmed-article:1309535 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:1309535 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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