Mauss S, Niederau C, Hengels K J
Department of Gastroenterology, Heinrich-Heine University Duesseldorf, Germany.
Anticancer Res. 1994 Jan-Feb;14(1A):215-20.
Gastrin-17 stimulated growth of the human colon carcinoma cell line HT29 but not of the human colon carcinoma cell lines T84, HCT116 and the mouse fibroblast cell line 3T3-L1. Correspondingly, specific gastrin binding sites were only found on HT29-cells. Proglumide, loxiglumide and L-365,260 inhibited gastrin-17 stimulated growth of HT29-cells at doses which did not influence cell growth when given without gastrin. At higher concentrations proglumide and loxiglumide reduced cell proliferation in all cell lines investigated. Gastrin-17 could not reverse these effects. This growth inhibition was therefore considered as not gastrin receptor mediated. The results demonstrate that only some human colon carcinoma cell lines are stimulated by gastrin. This stimulation can be inhibited by gastrin/CCK-antagonists.
胃泌素-17可刺激人结肠癌细胞系HT29生长,但对人结肠癌细胞系T84、HCT116及小鼠成纤维细胞系3T3-L1无刺激作用。相应地,仅在HT29细胞上发现了特异性胃泌素结合位点。丙谷胺、洛谷胺和L-365,260在不影响细胞生长的剂量下可抑制胃泌素-17对HT29细胞生长的刺激作用,若单独给药则无此影响。在更高浓度下,丙谷胺和洛谷胺可降低所有所研究细胞系的细胞增殖。胃泌素-17无法逆转这些作用。因此,这种生长抑制被认为不是由胃泌素受体介导的。结果表明,仅部分人结肠癌细胞系受胃泌素刺激,这种刺激可被胃泌素/胆囊收缩素拮抗剂抑制。