Aberrant MYCN expression drives oncogenic hijacking of EZH2 as a transcriptional activator in peripheral T-cell lymphoma

Blood. 2022 Dec 8;140(23):2463-2476. doi: 10.1182/blood.2022016428.

Abstract

Peripheral T-cell lymphoma (PTCL) is a heterogeneous group of hematological cancers arising from the malignant transformation of mature T cells. In a cohort of 28 PTCL cases, we identified recurrent overexpression of MYCN, a member of the MYC family of oncogenic transcription factors. Approximately half of all PTCL cases was characterized by a MYC expression signature. Inducible expression of MYCN in lymphoid cells in a mouse model caused T-cell lymphoma that recapitulated human PTCL with an MYC expression signature. Integration of mouse and human expression data identified EZH2 as a key downstream target of MYCN. Remarkably, EZH2 was found to be an essential cofactor for the transcriptional activation of the MYCN-driven gene expression program, which was independent of methyltransferase activity but dependent on phosphorylation by CDK1. MYCN-driven T-cell lymphoma was sensitive to EZH2 degradation or CDK1 inhibition, which displayed synergy with US Food and Drug Administration-approved histone deacetylase (HDAC) inhibitors.

MeSH terms

  • Enhancer of Zeste Homolog 2 Protein* / genetics
  • Humans
  • Lymphoma, T-Cell, Peripheral* / genetics
  • N-Myc Proto-Oncogene Protein* / genetics

Substances

  • Enhancer of Zeste Homolog 2 Protein
  • EZH2 protein, human
  • MYCN protein, human
  • N-Myc Proto-Oncogene Protein