...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cancer Cell >Loss of FBP1 by Snail-Mediated Repression Provides Metabolic Advantages in Basal-like Breast Cancer.
【24h】

Loss of FBP1 by Snail-Mediated Repression Provides Metabolic Advantages in Basal-like Breast Cancer.

机译：蜗牛介导的阻抑导致FBP1的丧失为基础型乳腺癌提供了代谢优势。

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 epithelial-mesenchymal transition (EMT) enhances cancer invasiveness and confers tumor cells with cancer stem cell (CSC)-like characteristics. We show that the Snail-G9a-Dnmt1 complex, which is critical for E-cadherin promoter silencing, is also required for the promoter methylation of fructose-1,6-biphosphatase (FBP1) in basal-like breast cancer (BLBC). Loss of FBP1 induces glycolysis and results in increased glucose uptake, macromolecule biosynthesis, formation of tetrameric PKM2, and maintenance of ATP production under hypoxia. Loss of FBP1 also inhibits oxygen consumption and reactive oxygen species production by suppressing mitochondrial complex I activity; this metabolic reprogramming results in an increased CSC-like property and tumorigenicity by enhancing the interaction of β-catenin with T-cell factor. Our study indicates that the loss of FBP1 is a critical oncogenic event in EMT and BLBC.
机译：上皮-间质转化（EMT）增强了癌症的侵袭性，并使肿瘤细胞具有类似于癌症干细胞（CSC）的特征。我们显示，Snail-G9a-Dnmt1复合物，对于E-钙粘蛋白启动子沉默至关重要，对于基础样乳腺癌（BLBC）中的果糖-1,6-双磷酸酶（FBP1）的启动子甲基化也是必需的。 FBP1的丢失会诱导糖酵解，并导致葡萄糖摄取增加，大分子生物合成，四聚体PKM2的形成以及在缺氧条件下维持ATP的产生。 FBP1的丢失还通过抑制线粒体复合物I的活性来抑制耗氧量和活性氧的产生;通过增强β-catenin与T细胞因子的相互作用，这种代谢重编程可提高CSC样特性和致瘤性。我们的研究表明FBP1的丢失是EMT和BLBC中的关键致癌事件。

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