Gastrin and pentagastrin enhance the tumour proliferation of human stable cultured gastric adenocarcinoma cells

The effect of gastrin on stimulating tumour proliferation has been evaluate d on human pancreas cancer cells in culture and in tumours transplanted to nude mice. The presence of CCK-B/gastrin-like receptor responsible for that effect of gastrin has been proved in colonic (WiDr, HT-29, YAMC) and pancr eatic (PANC-1, BON) cell lines. The aim of our study was to examine the sti mulating effect of gastrin and pentagastrin on the growth of human gastric adenocarcinoma cell line. The human gastric adenocarcinoma cell line (AGS, CRL-1739) was purchased from ATCC (Rockville, MA, USA). Gastrin-17 was purc hased from Sigma-Aldrich (Budapest, Hungary), pentagastrin was from Zeneca Limited (Macclasfield, UK). The cells were incubated in DMEM containing 10% FCS on 96-well culturing plate with 10(4) cells/well starting cell number at 37 degrees C with 5% CO2. The proliferation rates were detected: by the measurements of the metabolically active cells with Owen's reagent and the determination of protein content, and by cell counting in a haemocytometer at several incubation times. As a result, we detected similar proliferation rates using gastrin-17 or pentagastrin in the incubation medium. The stimu lating effect of gastrin/pentagastrin on cell line proliferation was in cor relation with its concentration. Our results proved that pentagastrin is a 10 times less effective stimulator of proliferation of gastric cancer than gastrin-17, and that AGS human adenocarcinoma cell Line might be CCK recept or positive. (C) 2000 Elsevier Science Ltd. Published by Editions scientifi ques et medicales Elsevier SAS.