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Kazuhiko Imakawa, Rulan Bai, Hiroshi Fujiwara, Atsushi Ideta, Yoshito Aoyagi and Kazuya Kusama

( Wathes & Wooding 1980 ). Another surprising finding was that changes in gene expression associated with epithelial–mesenchymal transition (EMT) occurred not before attachment, but rather on day 22. EMT is known as the process characterized by

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Gordon J Allan, James Beattie and David J Flint

to the process of senescence. In the normal response to injury, epithelial cells not only undergo an epithelial–mesenchymal transition (EMT) and migrate over the wound site, but also exhibit a burst of proliferation to replace lost cells. Most cells

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Lori Cole, Miranda Anderson, Parker B Antin and Sean W Limesand

. Although the general changes in cell morphology that occur during this single cell migration (or ‘budding’) suggest that an epithelial–mesenchymal transition (EMT) is involved, the process has not been carefully defined in any species. EMT is an important

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Hyo-Sup Kim, Seung-Hyun Hong, Seung-Hoon Oh, Jae-Hyeon Kim, Myung-Shik Lee and Moon-Kyu Lee

earlier than ductal cells. Recent studies reported the switch of cell phenotype in epithelial cell culture, and this change was due to epithelial–mesenchymal transition (EMT). EMT plays an important role in dedifferentiation, proliferation, and

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Norbert Chauvet, Taoufik El-Yandouzi, Marie-Noëlle Mathieu, Audrey Schlernitzauer, Evelyne Galibert, Chrystel Lafont, Paul Le Tissier, Iain C Robinson, Patrice Mollard and Nathalie Coutry

. 1987 , Rukstalis & Habener 2007 ). Indeed, subtype switching is a prominent physiological feature of cadherin morphogenetic function during development, especially when epithelial–mesenchymal transition (EMT) takes place ( Halbleib & Nelson 2006

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Jin-Bong Lee, Sung-Jin Yoon, Sang-Hyun Lee, Moo-Seung Lee, Haiyoung Jung, Tae-Don Kim, Suk Ran Yoon, Inpyo Choi, Ik-Soo Kim, Su Wol Chung, Hee Gu Lee, Jeong-Ki Min and Young-Jun Park

45887 ) 10.1172/JCI45887 Tian L Shen D Li X Shan X Wang X Yan Q Liu J 2016 Ginsenoside Rg3 inhibits epithelial-mesenchymal transition (EMT) and invasion of lung cancer by down-regulating FUT4 . Oncotarget 7 1619

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Ankana Ganguly, Jennifer A Tamblyn, Sarah Finn-Sell, Shiao-Y Chan, Melissa Westwood, Janesh Gupta, Mark D Kilby, Stephane R Gross and Martin Hewison

novel and has been extensively reported in cancer states ( Krishnan et al . 2012 , Leyssens et al . 2014 , Ma et al . 2016 ), where effects of vitamin D have been related to modulation of epithelial–mesenchymal transition (EMT) ( Fischer & Agrawal

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Benoit Cox, Heleen Roose, Annelies Vennekens and Hugo Vankelecom

)land’ under basal conditions, but may become more ‘stormy’ in the stem cell compartment in the damage- and neonatally activated pituitary. EMT: preparing the pituitary stem cells for a stroll? Epithelial–mesenchymal transition (EMT) is a highly

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Sheree D Martin and Sean L McGee

through these mechanisms is essential for the epithelial–mesenchymal transition (EMT) and stemness of basal-like breast cancer cells ( Dong et al . 2013 ). These findings also imply that metabolic reprogramming is sufficient to induce breast cancer cell

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Alessandra Fierabracci

differentiated cells found in a cancer. Independent of the latest concept, the existence of other populations of cancer cells with special properties has been hypothesised. These include cells in epithelial–mesenchymal transition (EMT; Cannito et al . 2010