Devazepide (L-364718)抑制HT29-S-B6细胞的生长并增加肿瘤标志物的表达。

M E Forgue-Lafitte, A M Coudray, J P Aubert, C Gespach, J Bara
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引用次数: 0

摘要

Devazepide (L-364718, CCK-A受体的非肽拮抗剂)抑制粘液分泌、自主增殖的人结肠癌细胞系(HT29-S-B6)的增殖并诱导形态学改变。在指数生长阶段,添加10微米的地伐匹德(devazepide)至少3天,使胃M1粘蛋白的基线产量增加2-3倍,癌胚抗原的基线产量增加5倍。此外,地伐昔得诱导HT29-S-B6细胞表达MUC-5AC mRNA的量增加。替伐昔得引起的黏蛋白分泌增加在去除后是持续的,与血清的存在无关。综上所述,devazepd - l -364718在细胞克隆HT29-S-B6中具有成熟剂的作用。
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Devazepide (L-364718) inhibits growth and increases expression of tumor markers in HT29-S-B6 cells.

Devazepide (L-364718, a non-peptide antagonist of CCK-A receptors), inhibits the proliferation and induces morphologic changes in the mucous-secreting, autonomously proliferating human cancer colon cell line (HT29-S-B6. Addition of devazepide (10 microM) for at least 3 days in the exponential phase of growth enhanced the baseline production of gastric M1 mucins 2-3-fold and that of carcinoembryonic antigens 5-fold. Moreover, devazepide induced an increase in the amount of the MUC-5AC mRNA expressed by HT29-S-B6 cells. The increased in mucins secretion induced by devazepide was persistent after removal and independent of the presence of serum. In conclusion, devazepide-L-364718 behaves as a maturation agent in the cell clone HT29-S-B6.

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