...
首页> 外文期刊>Cell cycle >The disruption of the protein complex mutantp53/p73 increases selectively the response of tumor cells to anticancer drugs.
【24h】

The disruption of the protein complex mutantp53/p73 increases selectively the response of tumor cells to anticancer drugs.

机译:蛋白复合物突变体p53 / p73的破坏选择性地增加了肿瘤细胞对抗癌药物的反应。

获取原文
获取原文并翻译 | 示例
           

摘要

Many in vitro and in vivo evidence have shown that the status of p53 is a key determinant in the response of tumor cells to anticancer treatment. Here we provide evidence that peptide-mediated targeting of the protein complex mutantp53/p73 enhances the response of mutant p53 tumor cells to commonly used anticancer drugs. Indeed, we show that the disruption of the protein complex mutantp53/p73 and the consequent restoration of p73 transcriptional effects, through the activity of short interfering peptides, render mutant p53 cells more prone to the killing of adriamycin and cisplatin. Of note, the activity of the short interfering peptides is mutant p53 specific and causes no effects on wt-p53 and p53 null cells. Our findings highlight the protein complex mutantp53/p73 as a molecular target, whose successful overriding through the selective activity of small interfering peptides, might contribute to the optimization of mutant p53 tumor treatments.
机译:许多体外和体内证据表明,p53的状态是肿瘤细胞对抗癌治疗反应的关键决定因素。在这里,我们提供了蛋白质复合物突变体p53 / p73的肽介导靶向增强了突变体p53肿瘤细胞对常用抗癌药的反应的证据。确实,我们显示了通过短干扰肽的活性破坏蛋白复合物突变体p53 / p73和随后恢复p73转录作用,使得突变p53细胞更易于杀死阿霉素和顺铂。值得注意的是,短干扰肽的活性是突变体p53特异的,对wt-p53和p53空细胞没有影响。我们的研究结果突出了蛋白质复合物突变体p53 / p73作为分子靶标,其通过小分子干扰肽的选择性活性而被成功取代,可能有助于优化突变体p53肿瘤的治疗方法。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号