首页> 外文期刊>Cellular and molecular biology >OVEREXPRESSION OF MICRORNA-200c IN CD44+CD133+CSCS INHIBITS THE CELLULAR MIGRATORY AND INVASION AS WELL AS TUMORIGENICITY IN MICE
【24h】

OVEREXPRESSION OF MICRORNA-200c IN CD44+CD133+CSCS INHIBITS THE CELLULAR MIGRATORY AND INVASION AS WELL AS TUMORIGENICITY IN MICE

机译:MICRORNA-200c在CD44 + CD133 + CSCS中的过表达抑制小鼠细胞迁移和侵袭以及致突变性

获取原文
获取原文并翻译 | 示例
           

摘要

Cancer stem cells (CSCs) are believed to be responsible for drug resistance, metastasis of tumors. To investigate the biological characteristics of CD44+CD133+CSCs with over-expressing microRNA-200c (miR-200c), and to provide evidences for miR-200c as a tumor suppressor to treat melanoma. CD44+CD133+CSCs were isolated from the mouse melanoma B16F10 cell line by using immune magnetic activated cell sorting. The lentivirus miR-200c was transduced into the cells, and the effect of miR-200c overexpression on the biological characteristics of B16F10 CD44+ CD133+CSCs was analyzed by a series assays. The stable overexpression of miR-200c in B16F10 CD44+CD133+CSCs obviously resulted in downregulation of zinc-finger E-box binding homeobox 1 expression, reduction of the cell proliferation, colony forming, cell migratory and invasion ability in vitro as well as tumorigenicity in vivo compared with those of the B16F10 cells and B16F10 non-CD44+ CD133+CSCs. These findings suggest that the miR-200c overexpression as a novel strategy to target therapy of melanoma CSCs.
机译:癌症干细胞(CSC)被认为是造成药物耐药性和肿瘤转移的原因。调查过表达microRNA-200c(miR-200c)的CD44 + CD133 + CSCs的生物学特性,并为miR-200c作为抑制黑色素瘤的肿瘤抑制因子提供证据。通过使用免疫磁激活细胞分选法从小鼠黑素瘤B16F10细胞系中分离出CD44 + CD133 + CSC。将慢病毒miR-200c转导到细胞中,并通过一系列试验分析了miR-200c过表达对B16F10 CD44 + CD133 + CSCs生物学特性的影响。 miR-200c在B16F10 CD44 + CD133 + CSC中的稳定过表达明显导致锌指E-box结合同源异型盒1的表达下调,体外细胞增殖,集落形成,细胞迁移和侵袭能力降低以及致瘤性与B16F10细胞和B16F10非CD44 + CD133 + CSC的体内相比。这些发现表明,miR-200c过表达是靶向治疗黑色素瘤CSC的新策略。

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