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Loss of PRDM11 promotes MYC-driven lymphomagenesis

Cathrine Kolster Fog1, Fazila Asmar2, Christophe Côme1

  • 1Biotech Research and Innovation Centre and Centre for Epigenetics, University of Copenhagen, Copenhagen, Denmark;

Blood
|December 16, 2014
PubMed

Insights

The previously uncharacterized PRDM11 gene acts as a tumor suppressor by regulating oncogenes. Loss of PRDM11 accelerates MYC-driven lymphoma, impacting patient survival in diffuse large B-cell lymphomas.

Area of Science:

  • Molecular Biology
  • Genetics
  • Cancer Research

Background:

  • The PR-domain (PRDM) gene family encodes transcriptional regulators implicated in cancer.
  • Functional screening is a valuable approach for identifying novel tumor suppressors.
  • Understanding PRDM gene deregulation is crucial for cancer therapy development.

Purpose of the Study:

  • To identify novel tumor suppressors within the PRDM gene family.
  • To investigate the role of the uncharacterized PRDM family member, Prdm11, in cancer.
  • To elucidate the mechanistic basis of Prdm11's function in lymphomagenesis.

Main Methods:

  • Functional screening approach to identify novel tumor suppressors.
  • In vivo studies using Prdm11 knockout mice and the Eµ-Myc mouse model.
  • Analysis of PRDM11-deficient diffuse large B-cell lymphomas (DLBCLs) patient data.
  • Genome-wide mapping of PRDM11 binding sites and transcriptome sequencing.

Main Results:

  • Depletion of Prdm11 collaborates with MYC overexpression, promoting oncogenesis.
  • Overexpression of PRDM11 inhibits proliferation and induces apoptosis.
  • Loss of Prdm11 accelerates MYC-driven lymphomagenesis in mice.
  • PRDM11-deficient DLBCL patients exhibit poorer survival and belong to the non-germinal center B-cell-like subtype.
  • PRDM11 binds to transcriptional start sites and regulates oncogenes like FOS and JUN.

Conclusions:

  • PRDM11 is characterized as a putative novel tumor suppressor.
  • PRDM11 controls the expression of key oncogenes, including FOS and JUN.
  • This study provides new mechanistic insights into B-cell lymphomagenesis and highlights PRDM11 as a potential therapeutic target.

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