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

Second messengers and phosphoproteins Pub Date : 1991-01-01

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

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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.

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苏拉明抑制血管活性肠肽(VIP)结合和VIP诱导的cAMP在两种人类癌细胞系中的积累。

抗虫药物suramin可抑制单放射性碘化VIP (125I-VIP)与两种人类癌细胞系HT 29-D4和IGR 39的结合，IC50为280微克/毫升。即使浓度高达1500微克/毫升，该药物也无法去除先前结合在两种细胞上的125I-VIP。125I-VIP结合位点和VIP结合位点分子量均不受药物预处理细胞的影响。1000微克/毫升苏拉明对VIP诱导的cAMP积累的抑制作用为56%至99%，这取决于VIP的浓度和用于实验的细胞系。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，在急性或慢性用药治疗中，苏拉明不影响两种细胞中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。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Second messengers and phosphoproteins

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