| pubmed-article:11149419 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11149419 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:11149419 | lifeskim:mentions | umls-concept:C0376358 | lld:lifeskim |
| pubmed-article:11149419 | lifeskim:mentions | umls-concept:C0334227 | lld:lifeskim |
| pubmed-article:11149419 | lifeskim:mentions | umls-concept:C0596637 | lld:lifeskim |
| pubmed-article:11149419 | lifeskim:mentions | umls-concept:C1514485 | lld:lifeskim |
| pubmed-article:11149419 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:11149419 | pubmed:dateCreated | 2001-1-8 | lld:pubmed |
| pubmed-article:11149419 | pubmed:abstractText | Previous studies have shown that calcitonin-like immunoreactive substances are secreted by primary prostate cells. Furthermore, exogenously added calcitonin stimulates proliferation of androgen-responsive LnCaP cells. To examine the possible effect of calcitonin on growth of invasive prostate cancer cells, we tested its effects on proliferation of PC-3M cells. Calcitonin stimulated DNA synthesis of PC-3M cells in a dose-dependent fashion, and also stimulated adenylyl cyclase and protein kinase C activities. To further delineate the role of these signaling cascades in proliferation of PC-3M prostate cancer cells, we selectively activated these pathways by transfecting cDNAs expressing constitutively active forms of either Gsalpha (Gsalpha-QL) or Gqalpha (Gqalpha-QL). cDNAs expressing wild-type forms of G-proteins (Gsalpha-WT and Gqalpha-WT) were used as vehicle controls. Gqalpha-QL transfectants exhibited growth inhibition and terminal differentiation. Those expressing Gsalpha-QL exhibited a dramatic increase in growth rate. Gsalpha-QL transfectants displayed an almost 3-fold increase in [3H]-thymidine incorporation and over a 4-fold increase in growth rate when compared with parental PC-3M cells or those expressing wild-type Gsalpha (Gsalpha-WT). The growth-promoting action of Gsalpha-QL could not be mimicked by either 8-bromo cAMP or forskolin. However, nifedipine, a calcium channel antagonist, potently and selectively inhibited DNA synthesis in Gsalpha-QL transfectants. These results suggest that the growth-promoting actions of Gsalpha on PC-3M cells may be mediated by nifedipine-sensitive proliferative events. | lld:pubmed |
| pubmed-article:11149419 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11149419 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11149419 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11149419 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11149419 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11149419 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11149419 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11149419 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:11149419 | pubmed:issn | 0020-7136 | lld:pubmed |
| pubmed-article:11149419 | pubmed:author | pubmed-author:ChienJJ | lld:pubmed |
| pubmed-article:11149419 | pubmed:author | pubmed-author:RAJAGG | lld:pubmed |
| pubmed-article:11149419 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11149419 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:11149419 | pubmed:volume | 91 | lld:pubmed |
| pubmed-article:11149419 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11149419 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11149419 | pubmed:pagination | 46-54 | lld:pubmed |
| pubmed-article:11149419 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:11149419 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11149419 | pubmed:articleTitle | Role of stimulatory guanine nucleotide binding protein (GSalpha) in proliferation of PC-3M prostate cancer cells. | lld:pubmed |
| pubmed-article:11149419 | pubmed:affiliation | Department of Molecular and Integrative Physiology, The University of Kansas Medical Center, Kansas City, USA. | lld:pubmed |
| pubmed-article:11149419 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11149419 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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