Abstract | BACKGROUND & AIMS: METHODS: Two human pancreatic cell lines MiaPaca-2 and Panc-1 were transfected stably with both CCK receptor subtypes. Effects of CCK on various growth parameters including DNA synthesis, nuclear labeling, and colony formation were evaluated. RESULTS: Cells expressing either receptor subtype, but not untransfected cells, bound ligand and mobilized Ca2+ in response to CCK. CCK treatment caused a sustained pronounced inhibition of anchorage-independent growth. Similarly, CCK treatment inhibited anchorage-dependent growth. Receptor activation caused a concentration and time-dependent reduction in [3H] thymidine incorporation and nuclear labeling in cells cultured anchored to a plastic substrate. However, these effects on anchorage-dependent growth were transient, suggesting cellular desensitization. CONCLUSIONS: These data indicate that both CCK receptor subtypes can mediate growth inhibitory responses in pancreatic cancer cell lines and raise the possibility that CCK exerts a predominant growth inhibitory action on human pancreatic cancer cells.
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Authors | K Detjen, M C Fenrich, C D Logsdon |
Journal | Gastroenterology
(Gastroenterology)
Vol. 112
Issue 3
Pg. 952-9
(Mar 1997)
ISSN: 0016-5085 [Print] United States |
PMID | 9041258
(Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- Receptors, Cholecystokinin
- DNA
- Sincalide
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Topics |
- Cell Division
(drug effects)
- DNA
(biosynthesis)
- Dose-Response Relationship, Drug
- Humans
- Pancreatic Neoplasms
(pathology)
- Receptors, Cholecystokinin
(analysis, genetics, physiology)
- Sincalide
(pharmacology)
- Tumor Cells, Cultured
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