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Siouda M, Dujardin AD, Barbollat-Boutrand L, et al. CDYL2 Epigenetically Regulates MIR124 to Control NF-κB/STAT3-Dependent Breast Cancer Cell Plasticity. iScience. 2020;23(6):101141doi: 10.1016/j.isci.2020.101141.
Siouda, M., Dujardin, A. D., Barbollat-Boutrand, L., Mendoza-Parra, M. A., Gibert, B., Ouzounova, M., Bouaoud, J., Tonon, L., Robert, M., Foy, J. P., Lavergne, V., Manie, S. N., Viari, A., Puisieux, A., Ichim, G., Gronemeyer, H., Saintigny, P., & Mulligan, P. (2020). CDYL2 Epigenetically Regulates MIR124 to Control NF-κB/STAT3-Dependent Breast Cancer Cell Plasticity. iScience, 23(6), 101141. https://doi.org/10.1016/j.isci.2020.101141
Siouda, Maha, et al. "CDYL2 Epigenetically Regulates MIR124 to Control NF-κB/STAT3-Dependent Breast Cancer Cell Plasticity." iScience vol. 23,6 (2020): 101141. doi: https://doi.org/10.1016/j.isci.2020.101141
Siouda M, Dujardin AD, Barbollat-Boutrand L, Mendoza-Parra MA, Gibert B, Ouzounova M, Bouaoud J, Tonon L, Robert M, Foy JP, Lavergne V, Manie SN, Viari A, Puisieux A, Ichim G, Gronemeyer H, Saintigny P, Mulligan P. CDYL2 Epigenetically Regulates MIR124 to Control NF-κB/STAT3-Dependent Breast Cancer Cell Plasticity. iScience. 2020 Jun 26;23(6):101141. doi: 10.1016/j.isci.2020.101141. Epub 2020 May 06. PMID: 32450513; PMCID: PMC7251929.
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iScience. 2020 Jun 26;23(6):101141. doi: 10.1016/j.isci.2020.101141. Epub 2020 May 06.

CDYL2 Epigenetically Regulates MIR124 to Control NF-κB/STAT3-Dependent Breast Cancer Cell Plasticity.

iScience

Maha Siouda, Audrey D Dujardin, Laetitia Barbollat-Boutrand, Marco A Mendoza-Parra, Benjamin Gibert, Maria Ouzounova, Jebrane Bouaoud, Laurie Tonon, Marie Robert, Jean-Philippe Foy, Vincent Lavergne, Serge N Manie, Alain Viari, Alain Puisieux, Gabriel Ichim, Hinrich Gronemeyer, Pierre Saintigny, Peter Mulligan

Affiliations

  1. Université de Lyon, Université Claude Bernard Lyon 1, INSERM 1052, CNRS 5286, Centre Léon Bérard, Cancer Research Center of Lyon, Lyon, France.
  2. Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), CNRS UMR 7104, INSERM U964, University of Strasbourg, Illkirch, France.
  3. Université de Lyon, Université Claude Bernard Lyon 1, INSERM 1052, CNRS 5286, Centre Léon Bérard, Cancer Research Center of Lyon, Lyon, France; Equipe Labellisée Ligue Contre le Cancer, LabEx DEVweCAN.
  4. Université de Lyon, Université Claude Bernard Lyon 1, INSERM 1052, CNRS 5286, Centre Léon Bérard, Cancer Research Center of Lyon, Lyon, France; Department of Maxillo-facial Surgery and Stomatology, Pitié-Salpétrière Hospital, Pierre et Marie Curie University Paris 6, Sorbonne Paris Cite University, AP-HP, Paris 75013, France.
  5. Synergie Lyon Cancer, Plateforme de Bioinformatique "Gilles Thomas", Centre Léon Bérard, 28 rue Lannec, Lyon 69008, France; INRIA Grenoble-Rhône-Alpes, 655 Avenue de l'Europe, Montbonnot-Saint-Martin 38330, France.
  6. Université de Lyon, Université Claude Bernard Lyon 1, INSERM 1052, CNRS 5286, Centre Léon Bérard, Cancer Research Center of Lyon, Lyon, France; Centre de Recherche en Cancérologie de Lyon (CRCL), Centre Léon Bérard, Epigenetics and Cancer Team, Cheney A, 5e étage, 28 rue Laennec, Lyon Cedex 08 69373, France. Electronic address: [email protected].

PMID: 32450513 PMCID: PMC7251929 DOI: 10.1016/j.isci.2020.101141

Abstract

Epigenetic deregulation of gene transcription is central to cancer cell plasticity and malignant progression but remains poorly understood. We found that the uncharacterized epigenetic factor chromodomain on Y-like 2 (CDYL2) is commonly over-expressed in breast cancer, and that high CDYL2 levels correlate with poor prognosis. Supporting a functional role for CDYL2 in malignancy, it positively regulated breast cancer cell migration, invasion, stem-like phenotypes, and epithelial-to-mesenchymal transition. CDYL2 regulation of these plasticity-associated processes depended on signaling via p65/NF-κB and STAT3. This, in turn, was downstream of CDYL2 regulation of MIR124 gene transcription. CDYL2 co-immunoprecipitated with G9a/EHMT2 and GLP/EHMT1 and regulated the chromatin enrichment of G9a and EZH2 at MIR124 genes. We propose that CDYL2 contributes to poor prognosis in breast cancer by recruiting G9a and EZH2 to epigenetically repress MIR124 genes, thereby promoting NF-κB and STAT3 signaling, as well as downstream cancer cell plasticity and malignant progression.

Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.

Keywords: Cancer; Functional Aspects of Cell Biology; Molecular Mechanism of Gene Regulation; Stem Cells Research

Conflict of interest statement

Declaration of Interests The authors have no conflicts of interest to declare.

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