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MYC acetylated lysine residues drive oncogenic cell transformation and regulate select genetic programs for cell

Matthew Hurd1, Jeffrey Pino1, Kay Jang1

  • 1Department of Biochemistry, University of California Riverside, Riverside, California 92521, USA.

Genes & Development
|October 18, 2023
PubMed

Insights

MYC acetylation by p300 and GCN5 is reversible and affects MYC protein stability and function. Specific acetylated lysine (AcK) sites are crucial for MYC-driven cancer cell transformation and tumorigenesis.

Area of Science:

  • Oncogenic transcription factors
  • Epigenetics
  • Cancer biology

Background:

  • MYC is a critical oncogenic transcription factor.
  • Acetylation of MYC by p300 and GCN5 is known, but its functional significance remains unclear.
  • The roles of specific acetylated lysine (AcK) residues in MYC function are not well understood.

Purpose of the Study:

  • To investigate the functional significance of MYC acetylation at specific lysine residues.
  • To determine the impact of MYC acetylation on its stability, gene regulation, and oncogenic activities.
  • To explore the potential of targeting MYC AcK sites for cancer therapy.

Main Methods:

  • Analysis of MYC acetylation in malignant and nonmalignant cells.
  • Site-directed mutagenesis (lysine-to-arginine substitutions) to assess the function of AcK sites.
  • Evaluation of MYC stability, proliferation, anchorage-independent growth, and tumorigenic activity in vitro and in vivo.

Main Results:

  • MYC acetylation at major sites (K148(149), K157(158), K323) is reversible and enhanced by oncogenic MYC overexpression.
  • Acetylation differentially affects MYC stability and controls gene-specific functions in processes like cell adhesion, apoptosis, and metabolism.
  • Individual AcK sites are essential for MYC-mediated malignant transformation, anchorage-independent growth, and in vivo tumorigenesis.

Conclusions:

  • MYC acetylation is a dynamic regulatory mechanism impacting MYC stability and function.
  • Specific AcK sites play critical, distinct roles in MYC's oncogenic activities.
  • Targeting MYC AcK site-specific signaling pathways presents a potential therapeutic strategy for MYC-driven cancers.
Keywords:
MYC oncoproteinlysine acetylationmalignant transformation

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