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

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

Research output: Contribution to journalArticle

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Abstract

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 (US)
Pages (from-to)782-790
Number of pages9
JournalGastroenterology
Volume113
Issue number3
DOIs
StatePublished - 1997

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Gastrins
Glycine
Stomach Neoplasms
Cholecystokinin A Receptor
Cholecystokinin B Receptor
Growth
Cholecystokinin
Cell Line
big gastrin
gastrin 17
Gastrin-Secreting Cells
Acinar Cells
Colonic Neoplasms
Cell Proliferation

ASJC Scopus subject areas

  • Gastroenterology

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Regulation of growth of human gastric cancer by gastrin and glycine- extended progastrin. / Iwase, K.; Evers, B. M.; Hellmich, Mark; Guo, Y. S.; Higashide, S.; Hong Jin Kim, Jin Kim; Townsend, Courtney.

In: Gastroenterology, Vol. 113, No. 3, 1997, p. 782-790.

Research output: Contribution to journalArticle

Iwase, K. ; Evers, B. M. ; Hellmich, Mark ; Guo, Y. S. ; Higashide, S. ; Hong Jin Kim, Jin Kim ; Townsend, Courtney. / Regulation of growth of human gastric cancer by gastrin and glycine- extended progastrin. In: Gastroenterology. 1997 ; Vol. 113, No. 3. pp. 782-790.
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abstract = "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.",
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T1 - Regulation of growth of human gastric cancer by gastrin and glycine- extended progastrin

AU - Iwase, K.

AU - Evers, B. M.

AU - Hellmich, Mark

AU - Guo, Y. S.

AU - Higashide, S.

AU - Hong Jin Kim, Jin Kim

AU - Townsend, Courtney

PY - 1997

Y1 - 1997

N2 - 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.

AB - 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.

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