...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Down-regulation of 14-3-3ζ suppresses anchorage-independent growth of lung cancer cells through anoikis activation
【24h】

Down-regulation of 14-3-3ζ suppresses anchorage-independent growth of lung cancer cells through anoikis activation

机译：14-3-3ζ的下调通过失活激活抑制肺癌细胞的锚定非依赖性生长

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 family of 14-3-3 proteins has emerged as critical regulators of diverse cellular responses under both physiological and pathological conditions. Here, we report an important role of 14-3-3ζ in tumori-genesis through a mechanism that involves anoikis resistance. 14-3-3ζ is up-regulated in a number of cancer types, including lung cancer. Through an RNAi approach using human lung adenocarcinoma-derived A549 cells as a model system, we have found that knockdown of a single ζ isoform of 14-3-3 is sufficient to restore the sensitivity of cancer cells to anoikis and impair their anchorage-independent growth. Enhanced anoikis appears to be mediated in part by up-regulated BH3-only proteins. Bad and Bim, coupled with decreased Mcl-1, resulting in the subsequent activation of Bax. This study suggests a model in which anchorage-independent growth of lung cancer cells requires the presence of 14-3-3ζ. This work not only reveals a critical role of 14-3-3ζ in anoikis suppression in lung cancer cells, but also identifies and validates 14-3-3ζ as a potential molecular target for anticancer therapeutic development.
机译：14-3-3蛋白家族已成为生理和病理条件下多种细胞反应的关键调节剂。在这里，我们报告了14-3-3ζ在肿瘤发生中的重要作用，其机制涉及到抗厌氧症。 14-3-3ζ在包括肺癌在内的许多癌症类型中上调。通过使用人肺腺癌衍生的A549细胞作为模型系统的RNAi方法，我们发现敲除14-3-3的单个ζ亚型足以恢复癌细胞对缺氧的敏感性并损害其锚定非依赖性增长。增强的厌氧症似乎部分由仅BH3上调的蛋白介导。 Bad和Bim，再加上Mcl-1降低，导致随后的Bax激活。这项研究提出了一个模型，其中不依赖锚定的肺癌细胞生长需要14-3-3ζ的存在。这项工作不仅揭示了14-3-3ζ在抑制肺癌细胞中的无神经反应中的关键作用，而且还鉴定并验证了14-3-3ζ作为抗癌治疗发展的潜在分子靶标。

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