Regulation of growth of human gastric cancer by gastrin and glycine- extended progastrin

K. Iwase, B. M. Evers, M. R. Hellmich, Y. S. Guo, S. Higashide, Jin Kim Hong Jin Kim, Jr Townsend

Research output: Contribution to journalArticlepeer-review

90 Scopus citations


Background and Aims: Gastrin (G-17) stimulates the growth of certain gastric and colon cancers mostly through gastrin/cholecystokinin (CCK)-B receptors. Glycine-extended gastrin (Gly-G) stimulates growth of a rat pancreatic acinar cell line; however, the effect of Gly-G on human gastric cancers is not known: The purpose of this study was to characterize the trophic effect of G-17 and Gly-G on two human gastric cancer cell lines, AGS and SIIA. Methods: Binding analyses were performed, and cell growth was assessed by counting cells over a time course. Results: G-17 stimulated growth of both AGS and SIIA cells. In AGS cells, gastrin/CCK-B receptor antagonists inhibited the effect of G-17 and competitively antagonized 125I-G-17 binding, whereas the CCK-preferring (CCK-A) receptor antagonists had no effect. In contrast, CCK-A receptor antagonists inhibited the stimulatory effect of G-17 in SIIA cells, whereas CCK-B receptor antagonists had no effect. Gly-G stimulated the growth of AGS and SIIA cells; neither the CCK-B nor the CCK-A receptor antagonists blocked this effect. Conclusions: G- 17 stimulates proliferation of AGS cells through the CCK-B receptor; however, G-17-mediated growth of SIIA acts through a CCK-A-like receptor. Furthermore, Gly-G stimulates growth of human gastric cancer cell lines, possibly through a receptor other than the CCK-B or CCK-A receptor.

Original languageEnglish
Pages (from-to)782-790
Number of pages9
Issue number3
StatePublished - 1997

ASJC Scopus subject areas

  • Hepatology
  • Gastroenterology


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