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作 者:孙涛[1] 钱家鸣[1] 陆国钧[1] 邵国红[1] 刘挺[1] 陈元方[1]
机构地区:[1]中国协和医科大学北京协和医院
出 处:《中华消化杂志》1994年第S1期7-10,共4页Chinese Journal of Digestion
基 金:国家科委"八五"课题
摘 要:用3H-胸腺嘧啶脱氧核苷掺入法研究了蛙皮素(bombesin,BOM)及其受体拮抗剂[D-Arg1,D-Phe5,D-Trp7,9,Leu11]-substanceP(BOM-A)对人胃癌细胞株SGC7901生长的影响,并通过测定细胞内三磷酸肌醇(IP3)含量,进一步观察蛙皮素对胃癌细胞的受体后细胞内信息传递途径。结果示:蛙皮系能明显促进人胃癌细胞株的生长,而蛙皮素受体拮抗剂[D-Arg1,D-phe5,D-Trp7,9,Leu11]-substanceP,能抑制蛙皮素对胃癌细胞的促生长作用。在无血清培养基中,上述受体拮抗剂对人胃癌细胞生长也有直接的抑制,提示蛙皮素对胃癌细胞有自分泌调节作用。蛙皮素对细胞生长的促进作用是通过磷酸肌醇途径,使细胞内IP3增加所致。In this study,the effect of bombesin and bombesin receptor antagonist(D-Arg1,D-Phe5,D- Trp7,9, Leu11)-Substance P on the growth of human gastric cancer cell line SGC7901 was investigated using 3H-TdR incoaporation as a parameter for cell growth. Cellular IP3(inositol 1,4,5-trisphosphate) in cytosol was measured after bombesin stimulation to study the possible post-receptor signal transduction pathway. The results indicated that bombesin significantly promoted the growth of human gastric cancer cell line SGC7901, and this effect could be inhibited by bombesin receptor antagonis. In serum-free medium, bombesin receptor antagonist inhibited the growth of human gastric cancer cells.The bombesin-stimulated increase in cellular IP3 suggested an autocrine regulatory role of bombesin. The growth promoting effect of bombesin was possibly through the induction of IP3.
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