Myc signaling via the ARF tumor suppressor regulates p53-dependent apoptosis and immortalization

Zindy, Frederique; Eischen, Christine M.; Randle, David H.; Kamijo, Takehiko; Cleveland, John L.; Sherr, Charles J.; Roussel, Martine F.

doi:10.1101/gad.12.15.2424

PreprintCited by 1,245Cancer-related Molecular PathwaysTelomeres, Telomerase, and SenescenceCell death mechanisms and regulation

Myc signaling via the ARF tumor suppressor regulates p53-dependent apoptosis and immortalization

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Zindy, Frederique, Eischen, Christine M., Randle, David H., Kamijo, Takehiko, Cleveland, John L., Sherr, Charles J., Roussel, Martine F.·1998·Genes & Development

DOI 10.1101/gad.12.15.2424PMC PMC317045

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Abstract

Establishment of primary mouse embryo fibroblasts (MEFs) as continuously growing cell lines is normally accompanied by loss of the p53 or p19(ARF) tumor suppressors, which act in a common biochemical pathway. myc rapidly activates ARF and p53 gene expression in primary MEFs and triggers replicative crisis by inducing apoptosis. MEFs that survive myc overexpression sustain p53 mutation or ARF loss during the process of establishment and become immortal. MEFs lacking ARF or p53 exhibit an attenuated apoptotic response to myc ab initio and rapidly give rise to cell lines that proliferate in chemically defined medium lacking serum. Therefore, ARF regulates a p53-dependent checkpoint that safeguards cells against hyperproliferative, oncogenic signals.

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p19Arf inhibits Mdm2-mediated degradation of p53 and is required for activation of p53 in response to aberrant cell cycle entry and oncogene activation.
“p19 Arf has been shown to inhibit Mdm2-mediated degradation of p53 (19-21) and is clearly required for activation of p53 in response to aberrant cell cycle entry (19) and oncogene activation (22-24).”
From Ink4a / Arf tumor suppressor does not modulate the degenerative conditions or tumor spectrum of the telomerase-deficient mouse (2007) · cites this paper as [22]
This paper is cited for the oncogene-activation part of the sentence, not the separate claims about Mdm2-mediated degradation or aberrant cell-cycle entry. In “Induction of ARF by myc” (page unavailable), Myc-induced p53 activation was significantly impaired in ARF-null cells, but p53 levels still rose twofold. The source therefore supports an important role for ARF, not an absolute requirement for p53 activation. (LLM, conf=0.87)
Experimental — accuracy not yet measured
Under stress such as oncogene activation, loss of Arf leaves Mdm2 deregulated and prevents effective p53 activation.
“However, under stressful conditions, such as when oncogenes are activated, loss of Arf results in deregulated Mdm2 and the inability of a cell to effectively activate p53 (Eischen, et al., 1999; Schmitt, et al., 1999; Zindy, et al., 1998).”
From The Mdm network and its regulation of p53 activities: a rheostat of cancer risk (2014) · cites this paper as Zindy, et al., 1998

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Authors: Zindy, F., Eischen, C. M., Randle, D. H., Kamijo, T., Cleveland, J. L., Sherr, C. J., & Roussel, M. F.
Affiliations: St. Jude Children's Research Hospital (US)
ORCID: Eischen, Christine M.
Kamijo, Takehiko
Cleveland, John L.
Sherr, Charles J.
Roussel, Martine F.
Venue: Genes & Development
Publisher: Cold Spring Harbor Laboratory
Published: 1998-08-01
Volume: 12
Issue: 15
Pages: 2424-2433
ISSN: 0890-9369 (ISSN-L)
1549-5477
DOI: 10.1101/gad.12.15.2424
PMC: PMC317045
OpenAlex: W2046958356
Cited by: 1,245
References: 60
Citations by year: 2026: 6 · 2025: 15 · 2024: 14 · 2023: 32 · 2022: 10 · 2021: 27 · 2020: 15 · 2019: 22 · 2018: 15 · 2017: 23 · 2016: 28 · 2015: 19 · 2014: 43 · 2013: 45 · 2012: 46
Type: posted content
Language: en
Open access: bronze
doi.org
Locations: Genes & Development (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: St. Jude Children's Research Hospital (CA21765)
American Lebanese Syrian Associated Charities (CA 21765)
National Institutes of Health (5r01ca056819-08, CA21765))
National Cancer Institute (CA-71907, CA56819, P30CA021765, P01CA071907)
National Institute of Diabetes and Digestive and Kidney Diseases (DK 44158, R01DK044158)
Topics: Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords: MYC signaling, ARF tumor suppressor, p53, apoptosis, cell immortalization, p19ARF, TP53 mutation, oncogenic transformation
MeSH terms: Animals, Cell Division, Cell Line, Humans, Models, Biological, Mutation, Proteins, Signal Transduction, Gene Expression, Genes, Tumor Suppressor, Genes, p53, Genes, myc, Apoptosis, Gene Deletion, Tumor Suppressor Protein p14ARF, Mice

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Myc signaling via the ARF tumor suppressor regulates p53-dependent apoptosis and immortalization

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