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Cancer and Metastasis Reviews

, Volume 35, Issue 4, pp 645–654 | Cite as

EMT, cell plasticity and metastasis

  • Christine L. Chaffer
  • Beatriz P. San Juan
  • Elgene Lim
  • Robert A. Weinberg
Article

Abstract

Carcinoma cells that are induced to suppress their epithelial features and upregulate mesenchymal gene expression programs acquire traits that promote an invasive and metastatic phenotype. This is achieved through the expression of a program termed the epithelial-to-mesenchymal transition (EMT)—a fundamental cell-biological process that plays key roles in embryogenesis and wound healing. Re-activation of the EMT during cancer promotes disease progression and enhances the metastatic phenotype by bestowing upon previously benign carcinoma cell traits such as migration, invasion, resistance to anoikis, chemoresistance and tumour-initiating potential. Herein, we discuss recent insights into the function of the EMT and cancer cell plasticity during cancer progression, with a focus on their role in promoting successful completion of the later stages of the metastatic cascade.

Keywords

EMT Cancer cell plasticity Metastasis Partial-EMT Tumor-initiating cells (TICs) 

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Copyright information

© Springer Science+Business Media New York 2016

Authors and Affiliations

  1. 1.Garvan Institute of Medical ResearchDarlinghurstAustralia
  2. 2.The Kinghorn Cancer Centre, St Vincent’s HospitalUniversity of New South WalesDarlinghurstAustralia
  3. 3.Whitehead Institute for Biomedical ResearchCambridgeUSA
  4. 4.Department of BiologyMassachusetts Institute of TechnologyCambridgeUSA
  5. 5.Massachusetts Institute of Technology Ludwig Center for Molecular OncologyCambridgeUSA

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