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10.1016/j.celrep.2016.02.034

http://scihub22266oqcxt.onion/10.1016/j.celrep.2016.02.034
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suck abstract from ncbi


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pmid26947068      Cell+Rep 2016 ; 14 (10): 2281-8
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  • Plasticity between Epithelial and Mesenchymal States Unlinks EMT from Metastasis-Enhancing Stem Cell Capacity #MMPMID26947068
  • Beerling E; Seinstra D; de Wit E; Kester L; van der Velden D; Maynard C; Schäfer R; van Diest P; Voest E; van Oudenaarden A; Vrisekoop N; van Rheenen J
  • Cell Rep 2016[Mar]; 14 (10): 2281-8 PMID26947068show ga
  • Forced overexpression and/or downregulation of proteins regulating epithelial-to-mesenchymal transition (EMT) has been reported to alter metastasis by changing migration and stem cell capacity of tumor cells. However, these manipulations artificially keep cells in fixed states, while in vivo cells may adapt transient and reversible states. Here, we have tested the existence and role of epithelial-mesenchymal plasticity in metastasis of mammary tumors without artificially modifying EMT regulators. In these tumors, we found by intravital microscopy that the motile tumor cells have undergone EMT, while their epithelial counterparts were not migratory. Moreover, we found that epithelial-mesenchymal plasticity renders any EMT-induced stemness differences, as reported previously, irrelevant for metastatic outgrowth, because mesenchymal cells that arrive at secondary sites convert to the epithelial state within one or two divisions, thereby obtaining the same stem cell potential as their arrived epithelial counterparts. We conclude that epithelial-mesenchymal plasticity supports migration but additionally eliminates stemness-enhanced metastatic outgrowth differences.
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