Abstract
The epithelial-to-mesenchymal transition (EMT) is a physiological process activated during early embryogenesis, which continues to shape tissues and organs later on. It is also hijacked by tumor cells during metastasis. The regulation of EMT has been the focus of many research groups culminating in the last few years and resulting in an elaborate transcriptional network buildup. However, the implication of epigenetic factors in the control of EMT is still in its infancy. Recent discoveries pointed out that histone variants, which are key epigenetic players, appear to be involved in EMT control. This review summarizes the available data on histone variants’ function in EMT that would contribute to a better understanding of EMT itself and EMT-related diseases.
Highlights
The authors observed a loss of macroH2A1 during epithelial-to-mesenchymal transition (EMT) induced by overexpression of the transcription factors SNAI1 (Snail) or TWIST1 (Twist). This suggested that macroH2A1 plays a role in EMT, and it appears to be involved in blocking EMT induction
Histone variants are used by the cells to shape and model the genome landscape at wish, which, in turn, controls major cellular events
This general function of histone variants is exemplified in the case of EMT
Summary
Many key steps during embryogenesis result in the formation of new cell types with unique features They become morphologically visible when individual cells or tissues are generated by cell delamination during a process called epithelial-to-mesenchymal transition (EMT) or by cell clustering and re-epithelialization during mesenchymal-to-epithelial transition (MET). The key event of a bona fide EMT is the downregulation of E-cadherin (E-cad) and the activation of N-cadherin (N-cad) expression that leads to a loss of cell polarity, adherent morphology, and of the epithelial gene signature [1,5]. In exchange, they acquire an unpolarized mesenchymal morphology combined with increased cell motility and a mesenchymal gene signature, observed by an increased fibronectin and vimentin expression [2]. In addition to orchestrating morphogenetic events during embryogenesis, the process of MET is utilized by disseminating tumor cells and required for colonization and the formation of metastasis at distant sites [1,3,10]
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