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10.1016/j.celrep.2016.02.034 http://scihub22266oqcxt.onion/10.1016/j.celrep.2016.02.034 C4802222!4802222 !26947068     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26947068 &cmd=llinks): Failed to open stream: HTTP request failed! 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Plasticity between Epithelial and Mesenchymal States Unlinks EMT from Metastasis-Enhancing Stem Cell Capacity |pdf=|usr=}}{{26947068 }} gab.com Text Plasticity between Epithelial and Mesenchymal States Unlinks EMT from Metastasis-Enhancing Stem Cell Capacity JO: Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=26947068 #FOAvip 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. Twit Text FOAVip Plasticity between Epithelial and Mesenchymal States Unlinks EMT from Metastasis-Enhancing Stem Cell Capacity ????Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=26947068 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26947068 #FOAvip English Wikipedia <ref>{{Cite pmid|26947068 }}</ref> 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 PMID26947068 show 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. |*Epithelial-Mesenchymal Transition [MESH] |Animals [MESH] |Antigens, Polyomavirus Transforming/genetics/metabolism [MESH] |Breast Neoplasms/etiology/metabolism/*pathology [MESH] |Cadherins/antagonists & inhibitors/genetics/metabolism [MESH] |Carcinoma, Ductal/etiology/metabolism/*pathology [MESH] |Disease Models, Animal [MESH] |Female [MESH] |Flow Cytometry [MESH] |Humans [MESH] |Immunohistochemistry [MESH] |Lung Neoplasms/pathology/secondary [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Mice, SCID [MESH] |Neoplastic Stem Cells/cytology/*metabolism [MESH] |RNA Interference [MESH] |RNA, Small Interfering/metabolism [MESH] |Real-Time Polymerase Chain Reaction [MESH]Plasticity between Epithelial and Mesenchymal States Unlinks EMT from (epmc).pdf DeepDyve Pubget Overpricing