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. 2020 Jun 25;12(2):89–106. doi: 10.1007/s13238-020-00741-7

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Glycosylation changes in TGF-β-induced EMT. During TGF-β-induced epithelial–mesenchymal transition (EMT), the epithelial cells lose their cell-cell contact and apical-basal polarity, acquiring a mesenchymal phenotype with enhanced motility and invasion ability. Upon EMT, epithelial markers including E-cadherin, β-catenin, claudin-1 and occludin are downregulated and mesenchymal markers such as N-cadherin, Vimentin, Fibronectin and Snail1/2 are increased. Glycosylation changes occur during EMT. Different types of changes are shown in the red-dashed boxes, highlighting changes in O-glycans and increased expression of branched, core fucosylated and sialylated N-glycans. In addition, the Lewis antigens (S-Le^X, S-Le^A and Le^Y) of N-glycans also upregulated within this process. The composition of the GSLs changed, as showed by the depletion of Gg4 or GM2 and expression of GM3 during TGF-β-induced EMT.