• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cancer Cell >An Integrin-Linked Machinery of Cytoskeletal Regulation that Enables Experimental Tumor Initiation and Metastatic Colonization
【24h】

An Integrin-Linked Machinery of Cytoskeletal Regulation that Enables Experimental Tumor Initiation and Metastatic Colonization

机译：整合素相关的细胞骨架调节机制，可进行实验性肿瘤启动和转移性定植

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

Recently extravasated metastatic cancer cells use the Rif/mDia2 actin-nucleating/polymerizing machinery in order to extend integrin β1-containing, filopodium-like protrusions (FLPs), which enable them to interact productively with the surrounding extracellular matrix; this process governs the initial proliferation of these cancer cells. Here, we identify the signaling pathway governing FLP lifetime, which involves integrin-linked kinase (ILK) and β-parvin, two integrin:actin-bridging proteins that block cofilin-mediated actin-filament severing. Notably, the combined actions of Rif/mDia2 and ILK/β-parvin/cofilin pathways on FLPs are required not only for metastatic outgrowth but also for primary tumor formation following experimental implantation. This provides one mechanistic explanation for how the epithelial-mesenchymal transition (EMT) program imparts tumor-initiating powers to carcinoma cells, since it enhances FLP formation through the activation of ILK/β-parvin/cofilin pathway.
机译：最近渗出的转移性癌细胞使用Rif / mDia2肌动蛋白成核/聚合机制来扩展含整合素β1的丝状样突起（FLP），从而使它们能够与周围的细胞外基质有效地相互作用。这个过程控制着这些癌细胞的初始增殖。在这里，我们确定了控制FLP寿命的信号通路，其中涉及整联蛋白连接的激酶（ILK）和β-parvin，这两种整联蛋白：肌动蛋白桥接蛋白，阻断cofilin介导的肌动蛋白丝切断。值得注意的是，Rif / mDia2和ILK /β-parvin/ cofilin途径对FLP的联合作用不仅需要转移的生长，而且需要实验植入后原发肿瘤的形成。这为上皮-间质转化（EMT）程序如何赋予癌细胞以肿瘤启动能力提供了一种机械的解释，因为它通过激活ILK /β-parvin/ cofilin途径增强了FLP的形成。

著录项

相似文献

  • 外文文献
  • 中文文献
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