Abstract
The epithelial to mesenchymal transition (EMT) is a biological process in which a non-motile epithelial cell changes to a mesenchymal phenotype with invasive capacities. This phenomenon has been well documented in multiple biological processes including embryogenesis, fibrosis, tumor progression and metastasis. The hallmark of EMT is the loss of epithelial surface markers, most notably E-cadherin, and the acquisition of mesenchymal markers including vimentin and N-cadherin. The downregulation of E-cadherin during EMT can be mediated by its transcriptional repression through the binding of EMT transcription factors (EMT-TFs) such as SNAIL, SLUG and TWIST to E-boxes present in the E-cadherin promoter. Additionally, EMT-TFs can also cooperate with several enzymes to repress the expression of E-cadherin and regulate EMT at the epigenetic and post- translational level. In this review, we will focus on epigenetic and post- translational modifications that are important in EMT. In addition, we will provide an overview of the various therapeutic approaches currently being investigated to undermine EMT and hence, the metastatic progression of cancer as well.
Highlights
Epithelial-mesenchymal transition (EMT) is a biological process in which non-motile, polarized epithelial cells undergo a series of biochemical alterations, becoming motile non-polarized mesenchymal cells with invasive capacity, resistance to apoptosis and altered biosynthesis of extracellular matrix (ECM) components
14-3-3σ binds to SNAIL and SNAIL can no longer function on E-cadherin [107]. These results suggest that protein kinase D1 (PKD1) acts as a tumor and metastasis suppressor as it regulates Snail-mediated EMT
EMT is a process in which tumor cells within the primary tumor lose their cell junctions and their epithelial morphology changes to fibroblastoid morphology
Summary
Epithelial-mesenchymal transition (EMT) is a biological process in which non-motile, polarized epithelial cells undergo a series of biochemical alterations, becoming motile non-polarized mesenchymal cells with invasive capacity, resistance to apoptosis and altered biosynthesis of extracellular matrix (ECM) components. The EMT program is activated by multiple signaling pathways as well as several epigenetic and post-translational modifications such as methylation, acetylation, phosphorylation, glycosylation, hydroxylation and SUMOylation. Epigenetic modifications including modification of histone protein tails, and DNA promoter regions, play a key role in regulating gene expression by defining whether chromatin at a given genomic locus will be transcriptionally active or inactive [22].
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