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Global mapping of c-Myc binding sites and target gene networks in human B cells

Karen I Zeller1, XiaoDong Zhao, Charlie W H Lee

  • 1Department of Medicine and The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

Proceedings of the National Academy of Sciences of the United States of America
|November 10, 2006
PubMed

Insights

This study identifies direct Myc targets in human B lymphoid tumors, revealing 668 regulated genes. These findings offer a framework for understanding how MYC drives tumorigenesis and controls cell growth.

Area of Science:

  • Molecular Biology
  • Genomics
  • Cancer Research

Background:

  • The protooncogene MYC (c-Myc) is crucial for cell growth, proliferation, and apoptosis.
  • MYC deregulation is implicated in tumorigenesis, but direct Myc-induced transcriptomes driving transformation remain unclear.

Purpose of the Study:

  • To perform a genome-wide characterization of direct Myc binding targets in a human B lymphoid tumor model.
  • To identify genes directly regulated by Myc and understand its role in transcriptional control.

Main Methods:

  • Utilized Chromatin Immunoprecipitation coupled with pair-end ditag sequencing analysis (ChIP-PET).
  • Integrated ChIP-PET data with gene expression profiles to identify direct Myc targets.

Main Results:

  • Myc potentially occupies over 4,000 genomic loci, primarily near proximal promoter regions and CpG islands.
  • Identified 668 direct Myc-regulated genes, including 48 transcription factors.
  • Myc acts as a central transcriptional hub controlling growth and proliferation.

Conclusions:

  • Provides the first global genomic view of Myc binding sites.
  • Offers insights into Myc-involved transcriptional circuitries and cis-regulatory modules.
  • Establishes a framework for understanding Myc-induced tumorigenesis mechanisms.

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