Gene Expression Of Gastrin-17 And Its Receptor In Pancreatic Tissue And Proliferative Effects Of Them On Pancreatic Adenocarcinoma Cell

Background. Pancreatic adenocarcinoma has a poor prognosis and none of currently available therapies including surgical and radiochemo-therapy offers a significant survival advantage. Gastrin-17(G-17), a trophic hormone, and its receptor exit in the gastrointestinal tract. It has been shown to promote the growth of both normal gastrointestinal mucosa as well as some malignant gastrointestinal tumors including colorectal carcinoma and gastric carcinoma. Gastrin releasing peptide (GRP) and its receptor (CCKb/gastrin receptor, CCKe/GR) are able to promote gastric carcinoma cell to excrete G-17. Recently, the research about G-17 fpcused on pancreatic adenocarcinoma. G-17 may be an important role in the proliferation of pancreatic adenocarcinoma.Objective. To confirm expression of G-17, CCKb/GR, GRP, GRPR mRNA in human pancreatic adenocarcinoma cell andevaluate the effect of G-17 and CCKB/GR antagonist on human pancreatic adenocarcinoma cell line.Methods and materials. The 13 patients were operated ( Whipple's operation) during the past six months. There were 8 female patients and 5 male patients .The pathologic diagnosis all were "pancreatic adenocarcinoma ".The tissue samples were numbered carcinoma group, borderline group and normal group .The human pancreatic adenocarcinoma cell lines AsPC-1, Bxpc-3, were grown in RPMI-1640 medium containing 10%FCS. G-17, CCKB/GR, GRP and GRPR mRNA were amplified by RT-PCR from the samples and the two cell lines. The MTT assay and flow cytometre (FCM) were used to evaluate effect of G-17 and the antagonist Proglumide (PGL) on AsPC-1 .Results. 13 samples express CCKB/GR ,6 samples express G-17 and GRPR, 10 samples express GRP. AsPC-1 expressed G-17, CCKB/GR, GRPR. Bxpc-3 did not expressed G-17, GRP, GRPR but CCKu/GR. G-17 (10-7 mol/L-1 )caused significant proliferation of unstimulated AsPC-1. Proglumide significantly inhibited the proliferative effects of G-17 but by itself had no effects on basal growth of the AsPC-1.Conclusion. Pancreatic adenocarcinoma cell can express G-17, CCKB /GR, GRPR and GRP mRNA. G-17 can promote proliferation of pancreatic adenocarcinoma cell with CCKB/GR while PGL can restrain the proliferation completely. It may offer a new method treatment for malignant pancreatic tumor.