Epithelial to mesenchymal transition (EMT) is a well-defined cellular process that was discovered in chicken embryos and described as "epithelial to mesenchymal transformation" [1]. During EMT, epithelial cells lose their epithelial features and acquire mesenchymal character with migratory potential. EMT has subsequently been shown to be essential for both developmental and pathological processes including embryo morphogenesis, wound healing, tissue fibrosis and cancer [2]. During the past 5 years, interest and study of EMT especially in cancer biology have increased exponentially due to the implied role of EMT in multiple aspects of malignancy such as cell invasion, survival, stemness, metastasis, therapeutic resistance and tumor heterogeneity [3]. Since the process of EMT in embryogenesis and cancer progression shares similar phenotypic changes, core transcription factors and molecular mechanisms, it has been proposed that the initiation and development of carcinoma could be attributed to abnormal activation of EMT factors usually required for normal embryo development. Therefore, developmental EMT mechanisms, whose timing, location, and tissue origin are strictly regulated, could prove useful for uncovering new insights into the phenotypic changes and corresponding gene regulatory control of EMT under pathological conditions. In this review, we initially provide an overview of the phenotypic and molecular mechanisms involved in EMT and discuss the newly emerging concept of epithelial to mesenchymal plasticity (EMP). Then we focus on our current knowledge of a classic developmental EMT event, neural crest cell (NCC) delamination, highlighting key differences in our understanding of NCC EMT between mammalian and non-mammalian species. Lastly, we highlight available tools and future directions to advance our understanding of mammalian NCC EMT.
Keywords: Delamination; Epithelial to mesenchymal transition; Mouse embryo; Neural crest cell.
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