Iwase K, Evers B M, Hellmich M R, Guo Y S, Higashide S, Kim H J, Townsend C M
Department of Surgery, University of Texas Medical Branch, Galveston, USA.
Gastroenterology. 1997 Sep;113(3):782-90. doi: 10.1016/s0016-5085(97)70172-0.
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.
Binding analyses were performed, and cell growth was assessed by counting cells over a time course.
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.
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.
胃泌素（G-17）主要通过胃泌素/胆囊收缩素（CCK）-B受体刺激某些胃癌和结肠癌的生长。甘氨酸延伸型胃泌素（Gly-G）可刺激大鼠胰腺腺泡细胞系的生长；然而，Gly-G对人胃癌的影响尚不清楚。本研究的目的是明确G-17和Gly-G对两种人胃癌细胞系AGS和SIIA的营养作用。
进行结合分析，并通过在一段时间内对细胞计数来评估细胞生长。
G-17刺激AGS和SIIA细胞的生长。在AGS细胞中，胃泌素/CCK-B受体拮抗剂抑制G-17的作用并竞争性拮抗125I-G-17的结合，而CCK偏好型（CCK-A）受体拮抗剂则无作用。相反，CCK-A受体拮抗剂抑制G-17对SIIA细胞的刺激作用，而CCK-B受体拮抗剂无作用。Gly-G刺激AGS和SIIA细胞的生长；CCK-B和CCK-A受体拮抗剂均不能阻断这种作用。
G-17通过CCK-B受体刺激AGS细胞的增殖；然而，G-17介导的SIIA细胞生长通过一种类似CCK-A的受体起作用。此外，Gly-G可能通过CCK-B或CCK-A受体以外的受体刺激人胃癌细胞系的生长。
