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. 2020 Dec 22;13(1):10. doi: 10.3390/cancers13010010

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Examples of HOX genes involved in the activation or inhibition of the epithelial to mesenchymal transition (EMT) in breast cancer. Epithelial cells present apical–basal polarity and are maintained together by tight junctions, adherens junctions and desmosomes. Hemidesmosomes maintain epithelial cells together with basement membrane. At the end of this process, epithelial cells present mesenchymal characteristics as the absence of apical–basal polarity and presence of motility capacity. HOXA5 is known to inhibit the EMT via upregulation of CDH1 in the adherens junctions, while HOXB7 induce the EMT downregulating the epithelial proteins: Claudin-1, Claudin-7, Claudin-4 and CDH1, and upregulating vimentin and α-SMA.