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Regulation of growth of human gastric cancer by gastrin and glycine-extended progastrin.
BACKGROUND & 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.[1]References
- Regulation of growth of human gastric cancer by gastrin and glycine-extended progastrin. Iwase, K., Evers, B.M., Hellmich, M.R., Guo, Y.S., Higashide, S., Kim, H.J., Townsend, C.M. Gastroenterology (1997)
