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Differential Expression of Cholecystokinin Receptors and Their Ligands in Normal and Neoplastic Pancreas
Author(s) -
Ortega Emily E,
Smith Jill P.
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.915.16
Subject(s) - gastrin , pancreas , cholecystokinin , medicine , cholecystokinin receptor , endocrinology , pancreatic cancer , bombesin , biology , receptor , gastrin releasing peptide , secretin , gastrointestinal hormone , peptide hormone , cancer , neuropeptide , secretion
Background The gastrointestinal peptide gastrin has been identified in fetal pancreas where it is thought to play a role in growth and differentiation. Gastrin has also been identified as a growth factor that stimulates pancreatic cancer through the CCK‐B and CCK‐C receptors by an autocrine mechanism. Hypothesis It is hypothesized that gastrin re‐expression is important to pancreatic carcinogenesis. Methods Endpoint RT‐PCR was performed on normal human pancreas mRNA to detect RNA levels of gastrin and CCK peptide. PCR products were visualized on an ethidium bromide stained gel after electrophoresis. Normal human pancreatic tissue samples were evaluated for gastrin and CCK by immunohistochemistry. Results The end‐point RT‐PCR showed significant levels of CCK‐B receptor and CCK peptide in normal pancreas samples. The gastrin end‐point RT‐PCR showed low levels in all of the normal pancreas samples. Gastrin immunoreactivity was not detected in normal pancreas, however, staining of the positive control was reactive; the negative control showed no staining. Conclusions Normal pancreas possesses the receptor CCK‐B and the peptide CCK. Gastrin is not present in normal pancreatic tissues, but is detected in neoplastic pancreatic samples. Therefore, the re‐expression of gastrin plays a pivotal role in the development of pancreatic cancer and could be a potential trigger to pancreatic carcinogenesis.