Cited by 1,188Cancer-related Molecular PathwaysGenomics and Chromatin DynamicsSignaling Pathways in Disease

The c-Myc target gene network

Dang, Chi V., O’Donnell, Kathryn A., Zeller, Karen I., Nguyen, Tam, Osthus, Rebecca C., Li, Feng·2006·Seminars in Cancer Biology

Abstract

For more than a decade, numerous studies have suggested that the c-Myc oncogenic protein is likely to broadly influence the composition of the transcriptome. However, the evidence required to support this notion was made available only recently, much to the anticipation of an eagerly awaiting field. In the past 5 years, many high-throughput screens based on microarray gene expression profiling, serial analysis of gene expression (SAGE), chromatin immunoprecipitation (ChIP) followed by genomic array analysis, and Myc-methylase chimeric proteins have generated a wealth of information regarding Myc responsive and target genes. From these studies, the c-Myc target gene network is estimated to comprise about 15% of all genes from flies to humans. Both genomic and functional analyses of c-Myc targets suggest that while c-Myc behaves as a global regulator of transcription, groups of genes involved in cell cycle regulation, metabolism, ribosome biogenesis, protein synthesis, and mitochondrial function are over-represented in the c-Myc target gene network. c-Myc also consistently represses genes involved in cell growth arrest and cell adhesion. The overexpression of c-Myc predisposes cells to apoptosis under nutrient or growth factor deprivation conditions, although the critical sets of genes involved remain elusive. Despite tremendous advances, the downstream target genes that distinguish between physiologic and tumorigenic functions of c-Myc remain to be delineated.

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Crossref · 10.1016/j.semcancer.2006.07.014

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  • The Myc-Max complex has two regulatory mechanisms: (1) Myc-Max binds to specific recognition sites (E-Box elements) in the promoter region to activate gene transcription; (2) Myc-Max heterodimer is indirectly recruited to DNA by zinc finger protein Miz-1, thus inhibiting Myc regulatory genes.

    “The Myc-Max complex has two regulatory mechanisms: (1) Myc-Max binds to specific recognition sites (E-Box elements) in the promoter region to activate gene transcription; (2) Myc-Max heterodimer is indirectly recruited to DNA by zinc finger protein Miz-1, thus inhibiting Myc regulatory genes.417”

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Authors
Dang, C. V., O’Donnell, K. A., Zeller, K. I., Nguyen, T., Osthus, R. C., & Li, F.
Affiliations
Johns Hopkins University (US)
Corresponding author
Dang, Chi V.
Venue
Seminars in Cancer Biology
Publisher
Elsevier BV
Published
2006-08
Volume
16
Issue
4
Pages
253-264
ISSN
1044-579X (ISSN-L)
OpenAlex
W2062348957
Cited by
1,188
References
134
Citations by year
2026: 33 · 2025: 38 · 2024: 72 · 2023: 77 · 2022: 68 · 2021: 86 · 2020: 63 · 2019: 66 · 2018: 58 · 2017: 60 · 2016: 62 · 2015: 53 · 2014: 60 · 2013: 57 · 2012: 62
FWCI
5.03
Type
journal article
Language
en
Open access
closed
Locations
  • Seminars in Cancer Biology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Johns Hopkins University
  • National Cancer Institute (CA 57341, R01CA057341, CA 51497)
Topics
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
Keywords
c-Myc, MYC target genes, gene regulatory networks, transcriptional regulation, cell cycle regulation, metabolism, ribosome biogenesis, mitochondrial function, growth arrest, cell adhesion, apoptosis, nutrient deprivation, growth factor deprivation, carcinogenesis
MeSH terms
Animals, Humans, Transcription, Genetic, Proto-Oncogene Proteins c-myc, Protein Interaction Mapping

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