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Myc and Omomyc functionally associate with the Protein Arginine Methyltransferase 5 (PRMT5) in glioblastoma cells

Maria Patrizia Mongiardi1, Mauro Savino2, Laura Bartoli2

  • 1Institute of Cell Biology and Neurobiology, National Research Council (IBCN-CNR), Rome, Italy.

Scientific Reports
|November 14, 2015
PubMed

Insights

The study reveals that the c-Myc inhibitor Omomyc and c-Myc protein both influence epigenetic modifications by interacting with PRMT5-MEP50. This finding highlights new roles for c-Myc in gene regulation and suggests potential therapeutic targets.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • The c-Myc oncoprotein is frequently dysregulated in human cancers, yet its precise functions remain incompletely understood.
  • Omomyc, a c-Myc inhibitor, has demonstrated significant anticancer effects in preclinical models by disrupting the c-Myc network and influencing gene expression.
  • Previous research indicates Omomyc's ability to impair c-Myc's DNA binding, retain transrepressive functions, and induce histone deacetylation.

Purpose of the Study:

  • To investigate the epigenetic mechanisms underlying c-Myc and Omomyc activity.
  • To elucidate the role of Omomyc in modulating chromatin structure and c-Myc target gene expression.
  • To identify novel interactions and functions of c-Myc at the epigenetic level.

Main Methods:

  • Utilized human glioblastoma and HEK293T cells to analyze epigenetic modifications.
  • Employed confocal microscopy to visualize co-localization of Omomyc, c-Myc, PRMT5, and specific histone marks.
  • Interfered with Protein Arginine Methyltransferase 5 (PRMT5) activity to assess its impact on gene regulation by Myc and Omomyc.

Main Results:

  • Both c-Myc and Omomyc were found to stimulate histone H4 symmetric dimethylation of arginine 3 (H4R3me2s).
  • c-Myc and Omomyc were consistently associated with PRMT5, the enzyme responsible for H4R3me2s, and its cofactor MEP50.
  • Omomyc co-localized with c-Myc, PRMT5, and H4R3me2s-enriched chromatin domains, indicating a role in modifying chromatin structure.
  • Disruption of PRMT5 activity impaired Myc-driven gene activation but restrained Omomyc-mediated gene repression.

Conclusions:

  • Omomyc actively modifies chromatin structure through association with a histone-modifying complex, providing new insights into its anticancer mechanism.
  • c-Myc recruits the PRMT5-MEP50 complex, leading to H4R3 symmetric di-methylation, suggesting previously unrecognized roles in gene expression regulation.
  • The interaction between c-Myc, PRMT5, and epigenetic modifications presents potential new therapeutic strategies for cancer treatment.

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