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乌苯美司激活乳腺癌细胞系YMB-S的E-钙黏蛋白介导的黏附作用。

Ubenimex activates the E-cadherin-mediated adhesion of a breast cancer cell line YMB-S.

作者信息

Fujioka S, Kohno N, Hiwada K

机构信息

Second Department of Internal Medicine, Ehime University School of Medicine.

出版信息

Jpn J Cancer Res. 1995 Apr;86(4):368-73. doi: 10.1111/j.1349-7006.1995.tb03066.x.

Abstract

It has been reported that ubenimex, a biological response modifier, has a direct anti-tumor effect. To clarify the mechanism involved, we examined the effects of ubenimex on the growth and adhesive property of a breast cancer cell line YMB-S. The cells proliferate in a floating manner without aggregation in normal complete medium. Ubenimex induced cell-cell and cell-surface adhesion of the cells accompanied with growth suppression. E-Cadherin localized at cell-cell contact sites of adhered cells, and anti-E-cadherin antibody inhibited the adhesion. Both Western blot analysis and binding assay disclosed that there was no apparent difference between E-cadherin levels of the cells before and after the treatment with ubenimex. These results indicate that ubenimex inhibits the proliferation of YMB-S cells and augments cell-to-cell adhesion through the induction of E-cadherin-mediated adhesion resulting from the functional activation of pre-expressed but inefficient E-cadherin.

摘要

据报道,生物反应调节剂乌苯美司具有直接的抗肿瘤作用。为阐明其作用机制,我们研究了乌苯美司对乳腺癌细胞系YMB-S生长和黏附特性的影响。在正常完全培养基中,这些细胞以悬浮方式增殖且不聚集。乌苯美司诱导细胞间和细胞表面黏附,并伴有生长抑制。E-钙黏蛋白定位于黏附细胞的细胞间接触部位,抗E-钙黏蛋白抗体可抑制黏附。蛋白质免疫印迹分析和结合试验均表明,乌苯美司处理前后细胞的E-钙黏蛋白水平无明显差异。这些结果表明,乌苯美司通过诱导由预表达但功能低效的E-钙黏蛋白功能激活所导致的E-钙黏蛋白介导的黏附,从而抑制YMB-S细胞的增殖并增强细胞间黏附。

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