EZH2 and KDM6B Expressions Are Associated with Specific Epigenetic Signatures during EMT in Non Small Cell Lung Carcinomas

The role of Epigenetics in Epithelial Mesenchymal Transition (EMT) has recently emerged. Two epigenetic enzymes with paradoxical roles have previously been associated to EMT, EZH2 (Enhancer of Zeste 2 Polycomb Repressive Complex 2 (PRC2) Subunit), a lysine methyltranserase able to add the H3K27me3 m...

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Bibliographic Details
Published in:Cancers 2020-12, Vol.12 (12), p.3649
Main Authors: Lachat, Camille, Bruyère, Diane, Etcheverry, Amandine, Aubry, Marc, Mosser, Jean, Warda, Walid, Herfs, Michaël, Hendrick, Elodie, Ferrand, Christophe, Borg, Christophe, Delage-Mourroux, Régis, Feugeas, Jean-Paul, Guittaut, Michaël, Hervouet, Eric, Peixoto, Paul
Format: Article
Language:English
Subjects:
Cancer
Cell adhesion & migration
CRISPR
Enzymes
Epigenetics
Gene expression
Genotype & phenotype
Histones
Human health sciences
Life Sciences
Lung cancer
Lung carcinoma
Lysine
Mesenchyme
Metastasis
Non-small cell lung carcinoma
Oncologie
Oncology
Polycomb group proteins
Proteins
Roles
Sciences de la santé humaine
Tumors
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Summary:The role of Epigenetics in Epithelial Mesenchymal Transition (EMT) has recently emerged. Two epigenetic enzymes with paradoxical roles have previously been associated to EMT, EZH2 (Enhancer of Zeste 2 Polycomb Repressive Complex 2 (PRC2) Subunit), a lysine methyltranserase able to add the H3K27me3 mark, and the histone demethylase KDM6B (Lysine Demethylase 6B), which can remove the H3K27me3 mark. Nevertheless, it still remains unclear how these enzymes, with apparent opposite activities, could both promote EMT. In this study, we evaluated the function of these two enzymes using an EMT-inducible model, the lung cancer A549 cell line. ChIP-seq coupled with transcriptomic analysis showed that EZH2 and KDM6B were able to target and modulate the expression of different genes during EMT. Based on this analysis, we described INHBB, WTN5B, and ADAMTS6 as new EMT markers regulated by epigenetic modifications and directly implicated in EMT induction.
ISSN:2072-6694
2072-6694
DOI:10.3390/cancers12123649