Loss of E-Cadherin Promotes Metastasis via Multiple Downstream Transcriptional Pathways

DOI PDF 被引用文献41件

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公開日
2008-05-15
DOI
  • 10.1158/0008-5472.can-07-2938
公開者
American Association for Cancer Research (AACR)

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<jats:title>Abstract</jats:title> <jats:p>Loss of the epithelial adhesion molecule E-cadherin is thought to enable metastasis by disrupting intercellular contacts—an early step in metastatic dissemination. To further investigate the molecular basis of this notion, we use two methods to inhibit E-cadherin function that distinguish between E-cadherin's cell-cell adhesion and intracellular signaling functions. Whereas the disruption of cell-cell contacts alone does not enable metastasis, the loss of E-cadherin protein does, through induction of an epithelial-to-mesenchymal transition, invasiveness, and anoikis resistance. We find the E-cadherin binding partner β-catenin to be necessary, but not sufficient, for induction of these phenotypes. In addition, gene expression analysis shows that E-cadherin loss results in the induction of multiple transcription factors, at least one of which, Twist, is necessary for E-cadherin loss–induced metastasis. These findings indicate that E-cadherin loss in tumors contributes to metastatic dissemination by inducing wide-ranging transcriptional and functional changes. [Cancer Res 2008;68(10):3645–53]</jats:p>

収録刊行物

  • Cancer Research

    Cancer Research 68 (10), 3645-3654, 2008-05-15

    American Association for Cancer Research (AACR)

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