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This, together with the interconnection between several core EMT-TFs 75– 78, provides robustness to the system as well as the potential to modulate epithelial plasticity in response to different environmental cues.
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The role of stromally derived microenvironmental epigenetic effectors in modulating epithelial growth, hormonal response, morphogenesis and epithelial plasticity is discussed.
It can be considered as a marker of profound epithelial plasticity [2].
Therapeutic approaches to EMT are still in their infancy and we don't know which protein or pathways we should target to block this profound epithelial plasticity.
Epithelial-mesenchymal transition (EMT) is a form of epithelial plasticity that is important in normal embryonic development and is co-opted in the progression of pathological conditions including fibrosis and cancer [51 54].
Many different, often crosstalking mechanisms cause EMT which comprises a wide spectrum of changes in epithelial plasticity.
Epithelial plasticity could be limited to relocalization of junctional proteins or to a more drastic epithelial to mesenchymal transition (EMT).
Another mechanism to control epithelial plasticity is regulating those pathways controlling EMT.
EMT can, therefore, be regarded as a complex manifestation of epithelial plasticity [ 3].
Madin-Darby Canine Kidney (MDCK) cells are widely used for studies of EMT and epithelial plasticity.
Thus, the role of epithelial plasticity will be an underlying theme throughout this review.
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