<scp>EMT</scp> and <scp>MET</scp>: necessary or permissive for metastasis?

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  • Mohit Kumar Jolly
    Center for Theoretical Biological Physics Rice University Houston TX USA
  • Kathryn E. Ware
    Duke Cancer Institute & Department of Medicine Duke University Medical Center Durham NC USA
  • Shivee Gilja
    Duke Cancer Institute & Department of Medicine Duke University Medical Center Durham NC USA
  • Jason A. Somarelli
    Duke Cancer Institute & Department of Medicine Duke University Medical Center Durham NC USA
  • Herbert Levine
    Center for Theoretical Biological Physics Rice University Houston TX USA

説明

<jats:p>Epithelial‐to‐mesenchymal transition (<jats:styled-content style="fixed-case">EMT</jats:styled-content>) and its reverse mesenchymal‐to‐epithelial transition (<jats:styled-content style="fixed-case">MET</jats:styled-content>) have been suggested to play crucial roles in metastatic dissemination of carcinomas. These phenotypic transitions between states are not binary. Instead, carcinoma cells often exhibit a spectrum of epithelial/mesenchymal phenotype(s). While epithelial/mesenchymal plasticity has been observed preclinically and clinically, whether any of these phenotypic transitions are indispensable for metastatic outgrowth remains an unanswered question. Here, we focus on epithelial/mesenchymal plasticity in metastatic dissemination and propose alternative mechanisms for successful dissemination and metastases beyond the traditional <jats:styled-content style="fixed-case">EMT</jats:styled-content>/<jats:styled-content style="fixed-case">MET</jats:styled-content> view. We highlight multiple hypotheses that can help reconcile conflicting observations, and outline the next set of key questions that can offer valuable insights into mechanisms of metastasis in multiple tumor models.</jats:p>

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