The DOI matches its Crossref record; 127 of the 127 references it cites were found in a registry or an index.
MYC and tumor metabolism: chicken and egg
Open accessAbstract
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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“Many tumors driven by oncogenic KRAS and its downstream effector, the transcription factor MYC, exhibit metabolic reprogramming to consume and rely more on glutamine for both catabolic to anabolic pathways55,56.”
From The metabolic landscape of RAS-driven cancers from biology to therapy (2021) · cites this paper as [56]
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2 retracted
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RetractedShi, Y., Yang, Y., Hoang, B. Q., Bardeleben, C., Holmes, B., Gera, J., & Lichtenstein, A. K. (2015) · Oncogene · doi:10.1038/onc.2015.156 · Cited by 68
RetractedUnderstanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation
Vander Heiden, M. G., Cantley, L. C., & Thompson, C. B. (2009) · Science · doi:10.1126/science.1160809 · Cited by 16,197
The Warburg Effect: How Does it Benefit Cancer Cells?
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The Biology of Cancer: Metabolic Reprogramming Fuels Cell Growth and Proliferation
DeBerardinis, R. J., Lum, J. J., Hatzivassiliou, G., & Thompson, C. B. (2008) · Cell Metabolism · doi:10.1016/j.cmet.2007.10.002 · Cited by 4,088
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Endoplasmic reticulum stress: cell life and death decisions
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The transcription factor Myc controls metabolic reprogramming upon T lymphocyte activation
Wang, R., Dillon, C. P., Shi, L. Z., Milasta, S., Carter, R., Finkelstein, D., McCormick, L. L., Fitzgerald, P., Chi, H., Munger, J., et al. (2011) · Immunity · doi:10.1016/j.immuni.2011.09.021 · Cited by 2,140 · cited 2×
“In activated T cells, MYC increases the expression of G6PDH, encoding for glucose-6phosphate dehydrogenase, which catalyzes the first reaction of the oxidative phase, and TKT, which encodes for transketolase, an enzyme of the non-oxidative branch (Wang et al, 2011).”
BackgroundInsights into RNA Biology from an Atlas of Mammalian mRNA-Binding Proteins
Castello, A., Fischer, B., Eichelbaum, K., Horos, R., Beckmann, B. M., Strein, C., Davey, N. E., Humphreys, D. T., Preiss, T., Steinmetz, L. M., et al. (2012) · Cell · doi:10.1016/j.cell.2012.04.031 · Cited by 2,132
Gao, P., Tchernyshyov, I., Chang, T.-C., Lee, Y.-S., Kita, K., Ochi, T., Zeller, K. I., De Marzo, A. M., Van Eyk, J. E., Mendell, J. T., et al. (2009) · Nature · doi:10.1038/nature07823 · Cited by 2,124
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“Besides promoting a high glycolytic rate, HIF-1α activation also inhibits oxidative phosphorylation by up-regulating genes, such as pyruvate dehydrogenase kinase 1 (PDK1) and LDH-A.”
BackgroundInfluentialPKM2, function and expression and regulation
Zhang, Z., Deng, X., Liu, Y., Liu, Y., Sun, L., & Chen, F. (2019) · Cell & Bioscience · doi:10.1186/s13578-019-0317-8 · Cited by 518
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The metabolic landscape of RAS-driven cancers from biology to therapy
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Immunity, Hypoxia, and Metabolism–the Ménage à Trois of Cancer: Implications for Immunotherapy
Riera-Domingo, C., Audigé, A., Granja, S., Cheng, W.-C., Ho, P.-C., Baltazar, F., Stockmann, C., & Mazzone, M. (2020) · Physiological Reviews · doi:10.1152/physrev.00018.2019 · Cited by 310
Metadata
- Authors
- Dejure, F. R., & Eilers, M.
- Affiliations
- University of Würzburg (DE)
- Corresponding author
- Eilers, Martin
- ORCID
- Eilers, Martin
- Venue
- The EMBO Journal
- Published
- 2017-12-01
- Volume
- 36
- Issue
- 23
- Pages
- 3409-3420
- ISSN
- 0261-4189 (ISSN-L)
- 1460-2075
- 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
- 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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