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Epigenomes 2019, 3(1), 1; https://doi.org/10.3390/epigenomes3010001

Epigenetic Regulation of EMT (Epithelial to Mesenchymal Transition) and Tumor Aggressiveness: A View on Paradoxical Roles of KDM6B and EZH2

1
Interactions Hôte-Greffon-Tumeur/Ingénierie Cellulaire et Génique, INSERM, EFS BFC, UMR1098, Univ. Bourgogne Franche-Comté, F-25000 Besançon, France
2
DImaCell Platform, Univ. Bourgogne Franche-Comté, F-25000 Besançon, France
3
EPIGENEXP Platform, Univ. Bourgogne Franche-Comté, F-25000 Besançon, France
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Received: 3 December 2018 / Revised: 14 December 2018 / Accepted: 17 December 2018 / Published: 20 December 2018
(This article belongs to the Special Issue Biological Methylation in Development and Cancer 2.0)
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Abstract

EMT (epithelial to mesenchymal transition) is a plastic phenomenon involved in metastasis formation. Its plasticity is conferred in a great part by its epigenetic regulation. It has been reported that the trimethylation of lysine 27 histone H3 (H3K27me3) was a master regulator of EMT through two antagonist enzymes that regulate this mark, the methyltransferase EZH2 (enhancer of zeste homolog 2) and the lysine demethylase KDM6B (lysine femethylase 6B). Here we report that EZH2 and KDM6B are overexpressed in numerous cancers and involved in the aggressive phenotype and EMT in various cell lines by regulating a specific subset of genes. The first paradoxical role of these enzymes is that they are antagonistic, but both involved in cancer aggressiveness and EMT. The second paradoxical role of EZH2 and KDM6B during EMT and cancer aggressiveness is that they are also inactivated or under-expressed in some cancer types and linked to epithelial phenotypes in other cancer cell lines. We also report that new cancer therapeutic strategies are targeting KDM6B and EZH2, but the specificity of these treatments may be increased by learning more about the mechanisms of action of these enzymes and their specific partners or target genes in different cancer types. View Full-Text
Keywords: cancer; EMT; metastasis; epigenetics; KDM6B; EZH2; H3K27 cancer; EMT; metastasis; epigenetics; KDM6B; EZH2; H3K27
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Lachat, C.; Boyer-Guittaut, M.; Peixoto, P.; Hervouet, E. Epigenetic Regulation of EMT (Epithelial to Mesenchymal Transition) and Tumor Aggressiveness: A View on Paradoxical Roles of KDM6B and EZH2. Epigenomes 2019, 3, 1.

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