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苏拉明抑制血管活性肠肽(VIP)与两种人类癌细胞系的结合以及VIP诱导的环磷酸腺苷(cAMP)积累。

Suramin inhibits vasoactive intestinal peptide (VIP) binding and VIP-induced cAMP accumulation into two human cancerous cell lines.

作者信息

Bellan C, Pic P, Marvaldi J, Fantini J, Pichon J

机构信息

Institut de Chimie Biologique, CNRS URA 202, Université D'Aix-Marseille I, France.

出版信息

Second Messengers Phosphoproteins. 1991;13(4):163-71.

PMID:1667418
Abstract

The antihelminthic drug suramin inhibits the binding of monoradioiodinated VIP (125I-VIP) to two human cancerous cell lines, namely HT 29-D4 and IGR 39 derived from a colic adenocarcinoma and a superficial melanoma respectively, with an IC50 of 280 micrograms/ml. The drug is not able to remove 125I-VIP previously bound to either types of cells even with concentration as high as 1500 micrograms/ml. Neither 125I-VIP binding nor VIP binding sites molecular weight are affected by pretreatment of the cells by the drug. Suramin at 1000 micrograms/ml inhibits by 56% to 99% the cAMP accumulation induced by VIP, depending on the VIP concentrations and the cell lines used for the experiments. On the contrary the drug does not have any effects on the cAMP accumulation induced by the beta receptor agonist isoproterenol. Also suramin does not affect the basal accumulation of cAMP in both types of cells either in acute or chronic treatment with the drug. We speculate that these observations may account, at least in part, for the in vivo and in vitro effects of VIP and suramin on cell proliferation and survival.

摘要

抗蠕虫药苏拉明抑制单放射性碘化血管活性肠肽(125I-VIP)与两种人类癌细胞系的结合,这两种细胞系分别是源自结肠腺癌的HT 29-D4和源自浅表黑色素瘤的IGR 39,半数抑制浓度(IC50)为280微克/毫升。即使药物浓度高达1500微克/毫升,该药物也无法去除先前与任何一种细胞类型结合的125I-VIP。药物预处理细胞对125I-VIP结合或VIP结合位点的分子量均无影响。1000微克/毫升的苏拉明可抑制由VIP诱导的环磷酸腺苷(cAMP)积累的56%至99%,这取决于VIP浓度以及用于实验的细胞系。相反,该药物对β受体激动剂异丙肾上腺素诱导的cAMP积累没有任何影响。此外,无论是急性还是慢性给予该药物,苏拉明均不影响这两种细胞类型中cAMP的基础积累。我们推测,这些观察结果可能至少部分解释了VIP和苏拉明在体内和体外对细胞增殖和存活的影响。

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