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首页> 外文期刊>Anticancer Research: International Journal of Cancer Research and Treatment >Synergistic effects of topoisomerase I inhibitor, SN38, on Fas-mediated apoptosis.
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Synergistic effects of topoisomerase I inhibitor, SN38, on Fas-mediated apoptosis.

机译：拓扑异构酶I抑制剂SN38对Fas介导的细胞凋亡的协同作用。

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摘要

Inhibitors of topoisomerase I, such as camptothecin, have proven to be among the most promising new classes of anti-neoplastic agents introduced into the clinical setting in recent years. Irinotecan (CPT-11) is one of the most widely used camptothecin analogs and is converted to form the active metabolite SN-38. The present study was designed to explore apoptosis induced by SN38 and anti-Fas antibody (CH11) in WR/Fas-SMS1 cells and its possible mechanisms. The results demonstrate that combination of SN38 and CH11 synergistically enhanced cell apoptosis in WR/Fas-SMS1 cells. Western blotting analysis showed that combination of SN38 and CH11 activated the ATM-Chk1-p53 pathway, increased protein expression of phospho-p53 and cleavaged caspase-3, but down-regulated expression of phospho-p21. Our data suggest that combination of SN38 and CH11 enhanced apoptosis through down-regulation of p21 phosphorylation. In conclusion, inhibition of p21 could be a new adjuvant approach in cancer therapy.
机译：拓扑异构酶I的抑制剂，例如喜树碱，已被证明是近年来引入临床的最有前景的新型抗肿瘤药物之一。伊立替康（CPT-11）是最广泛使用的喜树碱类似物之一，并被转化成活性代谢物SN-38。本研究旨在探讨SN38和抗Fas抗体（CH11）在WR / Fas-SMS1细胞中诱导的凋亡及其可能的机制。结果表明，SN38和CH11的组合可协同增强WR / Fas-SMS1细胞的细胞凋亡。蛋白质印迹分析表明，SN38和CH11的结合激活了ATM-Chk1-p53途径，增加了磷酸化p53和裂解的caspase-3的蛋白表达，但下调了磷酸化p21的表达。我们的数据表明，SN38和CH11的结合通过下调p21磷酸化增强了细胞凋亡。总之，抑制p21可能是癌症治疗中的新辅助方法。

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