Epithelial-to-Mesenchymal Transition: Epigenetic Reprogramming Driving Cellular Plasticity. Issue 12 (December 2017)

• Record Type: Journal Article
• Authors: Skrypek, Nicolas; Goossens, Steven; De Smedt, Eva; Vandamme, Niels; Berx, Geert
• Is Part Of: Trends in genetics. Volume 33:Issue 12(2017)
• Page Start: 943
• Page End: 959
• Publication Date: 2017-12
• Subjects: Genetics -- Periodicals; 576.5
• DOI: 10.1016/j.tig.2017.08.004
• Languages: English
• ISSNs: 0168-9525

Abstract

Abstract : Epithelial-to-mesenchymal transition (EMT) is a process in which epithelial cells lose their junctions and polarity to gain a motile mesenchymal phenotype. EMT is essential during embryogenesis and adult physiological processes like wound healing, but is aberrantly activated in pathological conditions like fibrosis and cancer. A series of transcription factors (EMT-inducing transcription factor; EMT-TF) regulate the induction of EMT by repressing the transcription of epithelial genes while activating mesenchymal genes through mechanisms still debated. The nuclear interaction of EMT-TFs with larger protein complexes involved in epigenetic genome modulation has attracted recent attention to explain functions of EMT-TFs during reprogramming and cellular differentiation. In this review, we discuss recent advances in understanding the interplay between epigenetic regulators and EMT transcription factors and how these findings could be used to establish new therapeutic approaches to tackle EMT-related diseases. Trends: EMT is a reversible and plastic process that plays pivotal roles in multiple physiological and pathological conditions. EMT is associated with vast epigenetic changes and its outcome is influenced by the epigenetic landscape of the cell of origin. The expression of EMT transcription factors (EMT-TFs), the core regulators of EMT machinery, is altered upon forced epigenetic modifications. Multiple physical interactions have been demonstrated between EMT-TFs and epigenetic modifiers, which partly can explain their roles in cell fate determinations. Targeting the epigenetic network to block EMT in disease progression appears a novel promising strategy for EMT-related pathologies.