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Myc-induced SUMOylation is a therapeutic vulnerability for B-cell lymphoma

Alexander Hoellein1, Mohammad Fallahi2, Stephanie Schoeffmann1

  • 1III. Medical Department, Technische Universität München, Munich, Germany;

Blood
|August 22, 2014
PubMed

Insights

Myc overexpression drives aggressive cancers by altering protein modification. Inhibiting SUMOylation, a key process, halts Myc-driven lymphoma growth and triggers tumor regression, offering a new therapeutic strategy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Myc oncogenic transcription factors (c-Myc, N-Myc, L-Myc) regulate cell growth, division, and metabolism.
  • Myc overexpression in cancer correlates with aggressive disease, partly via the ubiquitin-proteasome system.
  • The role of SUMOylation, a related posttranslational modification, in Myc-driven tumorigenesis was unexplored.

Purpose of the Study:

  • To investigate the role of SUMOylation in Myc-dependent tumorigenesis.
  • To determine if Myc regulates SUMOylation pathways.
  • To explore SUMOylation inhibition as a therapeutic strategy for Myc-driven lymphomas.

Main Methods:

  • Analysis of SUMOylation machinery gene expression in mouse and human Myc-driven lymphomas.
  • Genetic inhibition of SUMOylation in Myc-driven cancer models.
  • In vivo loss-of-function and pharmacologic studies.

Main Results:

  • Myc-driven lymphomas exhibit increased expression of SUMOylation regulators, leading to hyper-SUMOylation.
  • Inhibition of SUMOylation halts Myc-induced proliferation, causing cell-cycle arrest, polyploidy, and apoptosis.
  • Targeting SUMOylation leads to rapid regression of Myc-driven lymphoma in vivo.

Conclusions:

  • Myc regulates SUMOylation pathways, contributing to tumorigenesis.
  • SUMOylation is essential for Myc-driven lymphoma proliferation and survival.
  • Inhibition of SUMOylation is a promising therapeutic approach for lymphomas involving MYC.

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