Cited by 247Cancer, Hypoxia, and MetabolismPI3K/AKT/mTOR signaling in cancerMetabolism, Diabetes, and Cancer

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MYC and tumor metabolism: chicken and egg

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Dejure, Francesca R, Eilers, Martin·2017·The EMBO Journal

DOI 10.15252/embj.201796438PMC PMC5709748

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Abstract

Transcription factors of the MYC family are deregulated in the majority of all human cancers. Oncogenic levels of MYC reprogram cellular metabolism, a hallmark of cancer development, to sustain the high rate of proliferation of cancer cells. Conversely, cells need to modulate MYC function according to the availability of nutrients, in order to avoid a metabolic collapse. Here, we review recent evidence that the multiple interactions of MYC with cell metabolism are mutual and review mechanisms that control MYC levels and function in response to metabolic stress situations. The main hypothesis we put forward is that regulation of MYC levels is an integral part of the adaptation of cells to nutrient deprivation. Since such mechanisms would be particularly relevant in tumor cells, we propose that-in contrast to growth factor-dependent controls-they are not disrupted during tumorigenesis and that maintaining flexibility of expression is integral to MYC's oncogenic function.

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Retracted
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Authors: Dejure, F. R., & Eilers, M.
Affiliations: University of Würzburg (DE)
Corresponding author: Eilers, Martin
ORCID: Eilers, Martin
Venue: The EMBO Journal
Publisher: Springer Science and Business Media LLC
Published: 2017-12-01
Volume: 36
Issue: 23
Pages: 3409-3420
ISSN: 0261-4189 (ISSN-L)
1460-2075
DOI: 10.15252/embj.201796438
PMC: PMC5709748
OpenAlex: W2767348608
Cited by: 240
References: 127
Citations by year: 2026: 13 · 2025: 24 · 2024: 21 · 2023: 30 · 2022: 29 · 2021: 43 · 2020: 31 · 2019: 35 · 2018: 13
FWCI: 2.20
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: The EMBO Journal (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Deutsche Forschungsgemeinschaft (DFG222/12‐1)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Keywords: c-Myc, cancer metabolism, metabolic reprogramming, nutrient deprivation, metabolic stress, MYC regulation, carcinogenesis
MeSH terms: Forkhead Box Protein O1, Mechanistic Target of Rapamycin Complex 1, Animals, Glucose, Glutamine, Humans, Neoplasms, Nucleotides, Stress, Physiological, Biogenic Polyamines, Genes, myc, Proto-Oncogene Proteins c-myc, Apoptosis, Metabolic Networks and Pathways

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