Cholecystokinin-a receptor messenger RNA expression in human pancreatic cancer

• Published in: Journal of gastrointestinal surgery Vol. 3; no. 2; pp. 134 - 140
• Main Authors: Moonka, Ravi, Zhou, Weigong, Bell, Richard H.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01-03-1999; Springer Nature B.V
• Subjects: Adenocarcinoma - genetics; Adenocarcinoma - metabolism; Adenocarcinoma - pathology; Blotting, Southern; cholecystokinin; Gene Expression Regulation, Neoplastic; Humans; In Situ Hybridization; Pancreas; Pancreatic cancer; Pancreatic neoplasms; Pancreatic Neoplasms - genetics; Pancreatic Neoplasms - metabolism; Pancreatic Neoplasms - pathology; Receptor, Cholecystokinin A; Receptors, Cholecystokinin - genetics; Receptors, Cholecystokinin - metabolism; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger - biosynthesis; Tumor Cells, Cultured; cholecystokinin; Pancreatic neoplasms; in situ hybridization
• ISSN: 1091-255X; 1873-4626
• DOI: 10.1016/S1091-255X(99)80022-5

Cholecystokinin (CCK) is a gut peptide hormone known to stimulate postprandial gallbladder contraction and pancreatic enzyme secretion. It has also been shown to induce the growth of normal pancreas and of malignant and premalignant lesions in rodents. Although CCK has been shown to promote the growth of human adenocarcinoma cell lines, its role in the growth of human pancreatic adenocarcinomas in vivo is less clear. Localization of CCK receptors to neoplastic cells within resected human tissue specimens would be suggestive of its potential action as an in vivo promoter of human pancreatic cancer. Resected tissue specimens of pancreatic adenocarcinomas were therefore studied by both reverse transcriptase-polymerase chain reaction (RT-PCR) and in situ hybridization for the presence of CCK-A receptors. Ninety percent of studied tumors demonstrated CCK-A expression by RT-PCR, and this expression was localized to neoplastic cells by in situ hybridization. An increase in the expression of CCK receptors is a mechanism by which pancreatic malignancies may gain a significant growth stimulus.