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During EMT, cells lose their epithelial features of polarity and adhesion, gain mesenchymal properties, and exhibit increased motility.
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TGF- β1 is involved in cellular proliferation, redifferentiation, angiogenesis, and epithelial to mesenchymal transition (EMT), the process by which epithelial cells lose cell polarity and cell-to-cell adhesion, gaining migratory and invasive properties, and it has been associated with metastasis in prostate cancer models [ 37– 41].
This process is characterized by loss of cell polarity, decrease in cell cell adhesion and gain in migration ability.
During this step, a small proportion of epithelial tumor cells lose cell-cell adhesion and gain higher mobility, thus allowing them to invade the adjacent tissues [ 2, 3].
These tumor cells need to remodel their tight cell cell and cell matrix adhesion to gain migratory capabilities, and thus to invade adjacent tissues.
EMT was originally defined as a process of cellular reorganization essential for embryonic development, resulting in the loss of cell-to-cell adhesion, and gain of invasive and migratory mesenchymal properties.
In effect, these protein markers are known to induce EMT, a process by which epithelial cells lose their cell polarity and cell cell adhesion, and gain migratory and invasive properties, thereby becoming mesenchymal stem cells.
Importantly, during epithelial-to-mesenchymal transition (EMT), tumor cells acquire a phenotype that encompasses all these traits as EMT is characterized by a loss of cell polarity and adhesion and gain of motile characteristics.
Epithelial mesenchymal transition (EMT) is a process whereby epithelial cells lose cell-to-cell adhesion and gain mesenchymal phenotype characterised by repression of membrane proteins such as E-cadherin and β-catenin, and overexpression of nuclear β-catenin, N-cadherin, Snail and Twist (Brabletz et al, 2001; Blanco et al, 2002; Thiery, 2002; Peinado et al, 2007).
Epithelial mesenchymal transition (EMT) is characterised by the loss of cell-to-cell adhesion and gaining of mesenchymal phenotypes.
All these genes are part of EMT signatures [ 20], where EMT is a process by which epithelial cells lose their cell polarity and cell-cell adhesion while gaining migratory and invasive properties to become mesenchymal cells [ 21, 22].
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