| pubmed-article:8436441 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8436441 | lifeskim:mentions | umls-concept:C0243038 | lld:lifeskim |
| pubmed-article:8436441 | lifeskim:mentions | umls-concept:C0079460 | lld:lifeskim |
| pubmed-article:8436441 | lifeskim:mentions | umls-concept:C1518174 | lld:lifeskim |
| pubmed-article:8436441 | lifeskim:mentions | umls-concept:C0010531 | lld:lifeskim |
| pubmed-article:8436441 | lifeskim:mentions | umls-concept:C1522484 | lld:lifeskim |
| pubmed-article:8436441 | lifeskim:mentions | umls-concept:C0036525 | lld:lifeskim |
| pubmed-article:8436441 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:8436441 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:8436441 | lifeskim:mentions | umls-concept:C0871161 | lld:lifeskim |
| pubmed-article:8436441 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:8436441 | pubmed:dateCreated | 1993-3-23 | lld:pubmed |
| pubmed-article:8436441 | pubmed:abstractText | Expression of granulocyte-macrophage colony-stimulating factor (GM-CSF) by metastatic Lewis lung carcinoma cells (LLC-LN7) was previously shown to contribute to the maintenance of phenotypic characteristics associated with an increased capacity to metastasize. In the present study, pre-incubation of LLC-LN7 cells with neutralizing anti-GM-CSF antibodies diminished the capacity of the tumor cells to form experimental metastases after i.v. inoculation, while pre-incubation with recombinant GM-CSF (rGM-CSF) increased formation of metastases. In the presence of rGM-CSF, the LLC-LN7 cells exhibited an increased capacity to migrate, invade through a reconstituted basement membrane, and adhere to lung tissue. Studies to identify the signal transduction pathway through which GM-CSF enhanced the in vitro metastatic properties of the LLC-LN7 tumor cells implicated protein kinase A (PKA). Signaling through PKA was suggested by the demonstration that the stimulation of tumor-cell motility by GM-CSF was blocked in the presence of the adenylate cyclase inhibitor nicotinic acid, or the PKA inhibitors A3 or KT5720. In addition, the role of PKA as a signaling mechanism for GM-CSF was assessed by using REV-LN7 cells, which are LLC-LN7 cells that have been stably transfected with an expression vector encoding a mutant PKA RI alpha subunit and which, in turn, express a cAMP-resistant PKA. Adherence and invasion by the PKA-defective REV-LN7 cells were not stimulated by rGM-CSF, contrasting with the stimulation observed for wild-type LLC-LN7 cells. These data suggest that rGM-CSF can further enhance the in vitro metastatic characteristics of LLC-LN7 tumor cells and that this is dependent on signal transduction through PKA. | lld:pubmed |
| pubmed-article:8436441 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8436441 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8436441 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8436441 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:8436441 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8436441 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8436441 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8436441 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8436441 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:8436441 | pubmed:issn | 0020-7136 | lld:pubmed |
| pubmed-article:8436441 | pubmed:author | pubmed-author:YoungM RMR | lld:pubmed |
| pubmed-article:8436441 | pubmed:author | pubmed-author:YoungM EME | lld:pubmed |
| pubmed-article:8436441 | pubmed:author | pubmed-author:MatthewsJJ | lld:pubmed |
| pubmed-article:8436441 | pubmed:author | pubmed-author:WrightM AMA | lld:pubmed |
| pubmed-article:8436441 | pubmed:author | pubmed-author:LozanoYY | lld:pubmed |
| pubmed-article:8436441 | pubmed:author | pubmed-author:DjordjevicAA | lld:pubmed |
| pubmed-article:8436441 | pubmed:author | pubmed-author:DevataSS | lld:pubmed |
| pubmed-article:8436441 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8436441 | pubmed:day | 20 | lld:pubmed |
| pubmed-article:8436441 | pubmed:volume | 53 | lld:pubmed |
| pubmed-article:8436441 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8436441 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8436441 | pubmed:pagination | 667-71 | lld:pubmed |
| pubmed-article:8436441 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:8436441 | pubmed:meshHeading | pubmed-meshheading:8436441-... | lld:pubmed |
| pubmed-article:8436441 | pubmed:meshHeading | pubmed-meshheading:8436441-... | lld:pubmed |
| pubmed-article:8436441 | pubmed:meshHeading | pubmed-meshheading:8436441-... | lld:pubmed |
| pubmed-article:8436441 | pubmed:meshHeading | pubmed-meshheading:8436441-... | lld:pubmed |
| pubmed-article:8436441 | pubmed:year | 1993 | lld:pubmed |
| pubmed-article:8436441 | pubmed:articleTitle | Granulocyte-macrophage colony-stimulating factor stimulates the metastatic properties of Lewis lung carcinoma cells through a protein kinase A signal-transduction pathway. | lld:pubmed |
| pubmed-article:8436441 | pubmed:affiliation | Department of Research Services, Hines V.A. Hospital, Hines, IL 60141. | lld:pubmed |
| pubmed-article:8436441 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8436441 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:8436441 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:8436441 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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