Coexpression of gastrin and gastrin receptors (CCK-B and ΔCCK-B) in gastrointestinal tumour cell lines. Issue 6 (1st June 1998)

• Record Type: Journal Article
• Authors: McWilliams, D F; Watson, S A; Crosbee, D M; Michaeli, D; Seth, R
• Is Part Of: Gut. Volume 42:Issue 6(1998)
• Page Start: 795
• Page End: 798
• Publication Date: 1998-06-01
• Subjects: gastrin -- CCK-B -- ΔCCK-B -- RT-PCR -- gastrointestinal cell lines; Gastroenterology -- Periodicals; 616.33
• DOI: 10.1136/gut.42.6.795
• Languages: English
• ISSNs: 0017-5749

Abstract

Abstract : Background —The peptide hormone gastrin is a recognised growth factor for gastrointestinal (GI) tumour cells. Carboxyamidated gastrins bind to the cell surface gastrin/cholecystokinin B (CCK-B) receptor which can be expressed as either a normal or a truncated isoform (ΔCCK-B). Aims —To compare gastrin gene expression with ΔCCK-B and total CCK-B (both isoforms) gene expression in both GI and non-GI tract derived human tumour cell lines. Methods —Total RNA was extracted and gene expression was assayed by the reverse transcription-polymerase chain reaction followed by Southern blotting and hybridisation with specific oligo probes. Results —Gastrin was expressed by 5/5 gastric and 7/8 colorectal cell lines. Coexpression of gastrin CCK-B isoform was found in 80% of gastric and 75% of colorectal cell lines. Non-GI cell lines, with the exception of a lymphoblastic leukaemia cell line, showed no coexpression. The truncated receptor, ΔCCK-B, was shown in 3/5 gastric and 5/8 colorectal cell lines and was always coexpressed with gastrin. Conclusions —The truncated gastrin receptor, ΔCCK-B, is coexpressed with gastrin in 8/13 GI tumour cell lines. Gastrin and CCK-B receptor isoforms may be involved in maintaining autocrine/paracrine growth pathways in GI cancer cells.