...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cell biology international. >Anti-miR-155 oligonucleotide enhances chemosensitivity of U251 cell to taxol by inducing apoptosis
【24h】

Anti-miR-155 oligonucleotide enhances chemosensitivity of U251 cell to taxol by inducing apoptosis

机译：抗miR-155寡核苷酸通过诱导细胞凋亡增强U251细胞对紫杉醇的化学敏感性

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The oncogene, microRNA-155, is significantly elevated in GBM (glioblastoma multiforme), regulating multiple genes associated with cancer cell proliferation, apoptosis and invasiveness. Thus, miR-155 can theoretically become a target for enhancement of the chemotherapy in cancer. Down-regulating miR-155 to enhance the effect of taxol has not been studied in human GBM. Human GBM U251 cells were treated with taxol and the miR-155 inhibitor alone or in combination. IC50 values were dramatically decreased in cells treated with miR-155 inhibitor combined with taxol, to a greater extent than those treated with taxol alone. Furthermore, the miR-155 inhibitor significantly enhanced apoptosis in U251 cells. The data suggest that miR-155 blockage increased the chemosensitivity to taxol in GBM cells, making combined treatment an effective therapeutic strategy for controlling the growth by inhibiting EAG1 expression.
机译：致癌基因microRNA-155在GBM（多形胶质母细胞瘤）中显着升高，调节与癌细胞增殖，凋亡和侵袭性相关的多个基因。因此，miR-155在理论上可以成为增强癌症化学疗法的靶标。在人GBM中尚未研究下调miR-155以增强紫杉醇的作用。单独或组合用紫杉酚和miR-155抑制剂处理人GBM U251细胞。与单独用紫杉醇处理的细胞相比，用miR-155抑制剂联合紫杉醇处理的细胞的IC50值显着降低。此外，miR-155抑制剂可显着增强U251细胞的凋亡。数据表明，miR-155阻断可增加GBM细胞对紫杉醇的化学敏感性，从而使联合治疗成为通过抑制EAG1表达来控制生长的有效治疗策略。

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