Probing the Fifty Shades of EMT in Metastasis

Abstract

The involvement of epithelial-to-mesenchymal transition (EMT) in metastasis has long been under debate. Recent efforts to probe the occurrence and functional significance of EMT in clinical samples and animal models have produced exciting but sometimes conflicting findings. The diversity of EMT underlies the challenge in studying its role in metastasis.

Keywords: Epithelial-to-mesenchymal transition (EMT); cancer metastasis; in vivo tracing; plasticity.

Figure 1. The EMT spectrum

EMT can be triggered by a number of different initiating signals and downstream regulators. During this process, epithelial cells transition to different extents toward the fully mesenchymal phenotype by progressively acquiring mesenchymal features while losing epithelial traits. The intermediate or partial EMT states, in which cells express both epithelial and mesenchymal markers, have been suggested to exhibit higher plasticity and stemness [9], although more extensive research is needed to validate the pathological relevance of the hypothesis. The levels of expression of epithelial adhesion molecules, such as E-cadeherin, and mesenchymal markers, such as Fsp1 and Vimentin, are represented by numbers of brown lines and green dots, respectively.