Yoder D G, Moody T W
Peptides. 1987 Jan-Feb;8(1):103-7. doi: 10.1016/0196-9781(87)90171-9.
The binding of 125I-Bolton Hunter-cholecystokinin octapeptide (125I-BH-CCK-8) to small cell lung cancer cell lines was investigated. 125I-BH-CCK-8 bound with high affinity (Kd = 2.4 nM) to an apparent single class of sites (1700/cell) using cell line NCI-H209. Binding was time dependent and the ratio of specific/nonspecific binding was 8/1. Pharmacology studies indicated that gastrin, caerulein, CCK-33 and nonsulfated CCK-8 were potent inhibitors of specific 125I-BH-CCK-8 binding whereas CCK-26-32-NH2 was not. Because CCK receptors are present on small cell lung cancer cells, CCK may function as a regulatory peptide in this disease.
研究了125I-博尔顿·亨特-胆囊收缩素八肽(125I-BH-CCK-8)与小细胞肺癌细胞系的结合情况。使用细胞系NCI-H209,125I-BH-CCK-8以高亲和力(Kd = 2.4 nM)结合到一类明显的位点(1700个/细胞)。结合具有时间依赖性,特异性/非特异性结合比为8/1。药理学研究表明,胃泌素、蛙皮素、CCK-33和非硫酸化CCK-8是特异性125I-BH-CCK-8结合的有效抑制剂,而CCK-26-32-NH2则不是。由于小细胞肺癌细胞上存在CCK受体,CCK可能在这种疾病中作为一种调节肽发挥作用。