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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
18
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pubmed:dateCreated |
1990-10-9
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pubmed:abstractText |
Many reports emphasized the role of gastrin as growth factor on normal gastrointestinal mucosa and pancreas. In the present study, we analyzed the proliferative effects of cholecystokinin (CCK) and gastrin peptides on a rat tumoral pancreatic cell line, AR42J, which possesses both CCKA and CCKB receptor subtypes. The results showed a good correlation between the binding of gastrin to CCKB receptor [Kd 1.125 +/- 0.3 (SD) nM] and its ability to either induce ornithine decarboxylase activity [50% effective concentration, 0.6 +/- 0.3 nM] and [3H]-thymidine incorporation [50% effective concentration, 2 +/- 0.4 nM]. Furthermore, the ability of different cholecystokinin and gastrin antagonists such as proglumide and asperlicin derivatives (respectively, CR1409, CR1505, and L364,718) were tested. We found that all antagonists displaced 125I-labeled gastrin binding, with the following order of potencies: L364,718 greater than CR1409 greater than CR1505 greater than proglumide. Furthermore, the 50% inhibitory concentration of CR1409 and CR1505 to inhibit gastrin stimulated ornithine decarboxylase activity (an early event involved in cell proliferation) and [3H]thymidine incorporation were in agreement with their constants of inhibition (Ki) on gastrin binding. The L364,718 compound, at a concentration which fully occupied the CCKA without affecting the CCKB, had no effect on gastrin stimulated ornithine decarboxylase activity and [3H]thymidine incorporation. In addition, this compound appeared to be a full agonist on CCKB receptor. These results confirm the implication of the CCKB receptor in the proliferative response of AR42J cells to gastrin.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/DNA, Neoplasm,
http://linkedlifedata.com/resource/pubmed/chemical/Gastrins,
http://linkedlifedata.com/resource/pubmed/chemical/Glutamine,
http://linkedlifedata.com/resource/pubmed/chemical/Ornithine Decarboxylase,
http://linkedlifedata.com/resource/pubmed/chemical/Proglumide,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cholecystokinin,
http://linkedlifedata.com/resource/pubmed/chemical/Thymidine,
http://linkedlifedata.com/resource/pubmed/chemical/lorglumide,
http://linkedlifedata.com/resource/pubmed/chemical/loxiglumide
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0008-5472
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
50
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
5829-33
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:2393852-Animals,
pubmed-meshheading:2393852-DNA, Neoplasm,
pubmed-meshheading:2393852-Gastrins,
pubmed-meshheading:2393852-Glutamine,
pubmed-meshheading:2393852-Ornithine Decarboxylase,
pubmed-meshheading:2393852-Pancreatic Neoplasms,
pubmed-meshheading:2393852-Proglumide,
pubmed-meshheading:2393852-Rats,
pubmed-meshheading:2393852-Receptors, Cholecystokinin,
pubmed-meshheading:2393852-Thymidine,
pubmed-meshheading:2393852-Tumor Cells, Cultured
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pubmed:year |
1990
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pubmed:articleTitle |
Lorglumide and loxiglumide inhibit gastrin-stimulated DNA synthesis in a rat tumoral acinar pancreatic cell line (AR42J).
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pubmed:affiliation |
Institut National de la Santé et de la Recherche Medicale, Unité 151, C.H.U. Rangueil, Toulouse, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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