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Differential expression of gastrin, cholecystokinin-A and cholecystokinin-B receptor mRNA in human pancreatic cancer cell lines
Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Clinical Microbiology . Östergötlands Läns Landsting, Centre for Laboratory Medicine, Department of Molecular Biological Techniques.
Malmo Univ Hosp, Dept Surg, MAS, SE-20502 Malmo, Sweden Linkoping Univ Hosp, LMO, Mol Biol Lab, S-58185 Linkoping, Sweden.
2001 (English)In: Scandinavian Journal of Gastroenterology, ISSN 0036-5521, Vol. 36, no 7, 738-743 p.Article in journal (Refereed) Published
Abstract [en]

Background: It has been assumed that gastrin stimulates the growth of pancreatic cancer in an autocrine way through co-expression of gastrin and the cholecystokinin-B receptor (CCK-BR). However, pancreatic cancer cell lines established directly from patients have revealed a great heterogeneity in cell proliferation when exposed to CCK, gastrin and their receptor antagonists. The aim of this study was therefore to examine co-expression of CCK-A and CCK-B receptor (CCK-AR and CCK-BR), and gastrin mRNA as well as the secretion of CCK and gastrin peptides in these cell lines. Methods: Fourteen cell lines were established from primary pancreatic cancers or their metastases. Total RNA was isolated from the cell lines and reverse-transcribed into single-stranded cDNA. A PCR technique based on Tag polymerase-antibody interaction and CCK-AR, CCK-BR and gastrin-specific primers, followed by Southern blot analysis, were the methods used. The incubation mediums were analysed for the presence of secreted CCK/proCCK and gastrin/progastrin peptides by specific radioimmunoassays (RIA). Results: By means of nested Reverse-Transcribed Polymerase Chain Reaction (nested RT-PCR), combined with Southern blot analysis of the PCR amplified products, CCK-AR and gastrin mRNA co-expression was detected in cell Lines LPC-6p and LPC-10m, whereas CCK-BR and gastrin mRNA could be detected in cell lines LPC-8p and LPC-12m. A low level of secreted CCK peptides was detected in cell line LPC-6p. which also expressed CCK-AR mRNA. In no other cases were CCK or gastrin peptides detected in the cell culture mediums. Conclusion: The lack of CCK-BR and gastrin mRNA co-expression, and not detectable levels of secreted CCK and gastrin in culture media, does not lend support to the hypothesis that concomitant gene-expression of CCK receptors and gastrin or CCK are essential to maintaining pancreatic cancer cell proliferation.

Place, publisher, year, edition, pages
2001. Vol. 36, no 7, 738-743 p.
Keyword [en]
cholecystokinin (CCK), CCK-A receptor, CCK-B receptor, gastrin, gene expression, pancreatic cancer
National Category
Medical and Health Sciences
URN: urn:nbn:se:liu:diva-49227OAI: diva2:270123
Available from: 2009-10-11 Created: 2009-10-11 Last updated: 2011-01-13

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Monstein, Hans-Jurg
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Faculty of Health SciencesClinical Microbiology Department of Molecular Biological Techniques
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