Distinct Thresholds Govern Myc's Biological Output In Vivo
Open accessAbstract
Deregulated Myc triggers a variety of intrinsic tumor suppressor programs that serve to restrain Myc's oncogenic potential. Since Myc activity is also required for normal cell proliferation, activation of intrinsic tumor suppression must be triggered only when Myc signaling is oncogenic. However, how cells discriminate between normal and oncogenic Myc is unknown. Here we show that distinct threshold levels of Myc govern its output in vivo: low levels of deregulated Myc are competent to drive ectopic proliferation of somatic cells and oncogenesis, but activation of the apoptotic and ARF/p53 intrinsic tumor surveillance pathways requires Myc overexpression. The requirement to keep activated oncogenes at a low level to avoid engaging tumor suppression is likely an important selective pressure governing the early stages of tumor microevolution.
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Even small amounts of uncontrolled c-Myc can drive cell division and tumor formation without activating Arf/p53 or causing apoptosis.
“More recently, Murphy et al. demonstrated that low levels of deregulated c-Myc are sufficient to promote cell proliferation and tumorigenesis without engaging the Arf/p53 pathway or triggering apoptosis [78].”
From The p53 orchestra: Mdm2 and Mdmx set the tone (2010) · cites this paper as [78]
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- Authors
- Murphy, D. J., Junttila, M. R., Pouyet, L., Karnezis, A., Shchors, K., Bui, D. A., Brown-Swigart, L., Johnson, L., & Evan, G. I.
- Affiliations
- University of California, San Francisco (US)
- Genentech (US)
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2008-12
- Volume
- 14
- Issue
- 6
- Pages
- 447-457
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC2723751
- OpenAlex
- W2084780592
- Cited by
- 456
- References
- 52
- Citations by year
- 2026: 14 · 2025: 14 · 2024: 26 · 2023: 27 · 2022: 13 · 2021: 24 · 2020: 28 · 2019: 26 · 2018: 10 · 2017: 24 · 2016: 17 · 2015: 23 · 2014: 36 · 2013: 37 · 2012: 30
- FWCI
- 18.83
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (submittedVersion)
- Funders
- National Cancer Institute (R01CA106526, F32CA099363, CA099363, R01CA098018)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- c-Myc, tumor surveillance, apoptosis, ARF-p53 pathway, oncogene activation
- MeSH terms
- Animals, Cell Nucleus, Fibroblasts, Genotype, Humans, Mice, Transgenic, Neoplasms, Signal Transduction, Gene Expression Regulation, Neoplastic, Polymerase Chain Reaction, Tumor Suppressor Protein p53, Proto-Oncogene Proteins c-myc, Apoptosis, Cell Proliferation, Mice
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