目的探索胃泌素/胆囊收缩素受体环对胃癌细胞增殖迁移的影响。方法用免疫细胞化学方法检测人胃癌细胞SGC-7901、AGS和胃黏膜上皮细胞GES-1细胞中胆囊收缩素-B(CCKB)受体的表达。分别培养这3种细胞,用不同终浓度胃泌素(10、100nmol/L)处理细胞,以未加胃泌素的细胞为对照,用细胞划痕实验和四甲基偶氮唑盐比色法检测细胞的增殖迁移能力。结果胃癌细胞SGC-7901、AGS中CCKB受体表达强阳性,而GES-1细胞中CCKB受体表达弱阳性;不同浓度胃泌素处理细胞后,SGC-7901、AGS细胞的增殖迁移能力明显增强,而GES-1细胞无明显改变;对照组、10nmol/L胃泌素处理组及100nmol/L胃泌素处理组中SGC-7901细胞的相对增殖率分别为100%、191.13%、212.65%,AGS细胞的相对增殖率分别为100%、189.27%、209.19%,各组间差异均有统计学意义(P均〈0.01);而GES-1细胞的相对增殖率分别为100%、113.01%、116.12%,各组间差异无统计学意义(P均〉0.05)。结论CCKB受体表达水平的高低对胃泌素/CCKB受体环促进胃癌细胞的增殖和迁移起重要作用。
Objective To study the effects of gastrin/CCKB receptor loop on the proliferation and migration of human gastric carcinoma cell. Methods The expression of CCKB receptor was detected in human gastric cancer cell lines SGC- 7901 and AGS cells and gastric epithelial cell line GES-1 cells by immunocytochemical method. Afrer three cultured cells were treated with the final concentration of l0 nmol/L and 100 nmol/L gastrin, the cell proliferation and migration were studied by cell wound assay and MTT colorimetric assay. The cells without treatment of gastrin served as the controls. Re- suits The expression of CCKB receptor expressed strong positively in SGC-7901 and AGS cells and weak positively in GES-1 cells. Compared with the control cells, the abilities of the proliferation and migration were significantly increased in gastric cancer AGS and SGC-7901 cells, but had no significant change in GES-1 cells after treatment of gastrin with the fi- nal concentration of 10 nmol/L and 100 nmol/L. The relative proliferation rate was 100%, 191.13% and 212.65% in SGC-7901 cells and 100%, 189.27% and 209.19% in AGS cells in the control, 10 nmol/L and 100 nmol/L gastrin groups, respectively. The difference was statistically significant (all P 〈0.01 ). But the relative proliferation rate in GES-1 ceils was 100%, 113.01% and 116.12% in the control, 10 nmol/L and 100 nmol/L gastrin groups respectively, which had no statistically significance (all P 〉 0.05). Conclusion The expression level of CCKB receptor have an important role in the proliferation and migration of gastric cancer cells promoted by gastrin/CCKB receptor loop.