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The Role for Myc in Coordinating Glycolysis, Oxidative Phosphorylation, Glutaminolysis, and Fatty Acid Metabolism in Normal and Neoplastic Tissues
Open accessAbstract
That cancer cells show patterns of metabolism different from normal cells has been known for over 50 years. Yet, it is only in the past decade or so that an appreciation of the benefits of these changes has begun to emerge. Altered cancer cell metabolism was initially attributed to defective mitochondria. However, we now realize that most cancers do not have mitochondrial mutations and that normal cells can transiently adopt cancer-like metabolism during periods of rapid proliferation. Indeed, an encompassing, albeit somewhat simplified, conceptual framework to explain both normal and cancer cell metabolism rests on several simple premises. First, the metabolic pathways used by cancer cells and their normal counterparts are the same. Second, normal quiescent cells use their metabolic pathways and the energy they generate largely to maintain cellular health and organelle turnover and, in some cases, to provide secreted products necessary for the survival of the intact organism. By contrast, undifferentiated cancer cells minimize the latter functions and devote their energy to producing the anabolic substrates necessary to maintain high rates of unremitting cellular proliferation. Third, as a result of the uncontrolled proliferation of cancer cells, a larger fraction of the metabolic intermediates normally used by quiescent cells purely as a source of energy are instead channeled into competing proliferation-focused and energy-consuming anabolic pathways. Fourth, cancer cell clones with the most plastic and rapidly adaptable metabolism will eventually outcompete their less well-adapted brethren during tumor progression and evolution. This attribute becomes increasingly important as tumors grow and as their individual cells compete in a constantly changing and inimical environment marked by nutrient, oxygen, and growth factor deficits. Here, we review some of the metabolic pathways whose importance has gained center stage for tumor growth, particularly those under the control of the c-Myc (Myc) oncoprotein. We discuss how these pathways differ functionally between quiescent and proliferating normal cells, how they are kidnapped and corrupted during the course of transformation, and consider potential therapeutic strategies that take advantage of common features of neoplastic and metabolic disorders.
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“c-Myc is known as the master regulator of the metabolic network, affecting different metabolic processes and transactivating almost all genes that code for enzymes of glycolysis and one-carbon metabolism [35,36,37].”
From 20-Hydroxyecdysone Boosts Energy Production and Biosynthetic Processes in Non-Transformed Mouse Cells (2024) · cites this paper as [36]
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“Transcription factors c-Myc and ATF4 are two master-regulators of glycolysis, respiration, and one-carbon metabolism [44,45,46,49].”
From 20-Hydroxyecdysone Confers Antioxidant and Antineoplastic Properties in Human Non-Small Cell Lung Cancer Cells (2023) · cites this paper as [44]
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“In addition, Myc has a significant impact on cellular metabolism and promotes glycolysis, oxidative phosphorylation and a myriad of metabolic pathways required to assure cancer cells of a continued supply of energy and anabolic building blocks to support proliferation, survival, and metastasis (50).”
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“Unique to Hallmark, Myc, transcription factor E2 targets, and G2/M cell division checkpoint pathways, additional indicators of increased cellular proliferation, were upregulated in all datasets 30,37,38 (Fig.”
BackgroundEmerging roles of the chromatin remodeler MORC2 in cancer metabolism
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Soyasaponin Ba Alleviates Lipid Accumulation via Mitochondrial Remodeling: Multiomics Insights
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Promising Role of PKM2 in the Diagnosis and Prognosis of Ovarian Cancer
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“Early structural and biochemical studies identified redox-sensitive disulfide bonds within intermembrane space-exposed subunits of CI and CIII, suggesting that oxidative conditions may influence SCs assembly through conformational effects [28,54–56].”
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“…CAFs by altering metabolic stress within the TME. c-Myc is a central transcription factor that regulates glycolysis, oxidative phosphorylation, glutamine metabolism, and lipid metabolism in tumor cells, thereby affecting their energy supply, biosynthetic capacity, and proliferative potential [87].”
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“This “forced metabolic normalization” likely reflects the preservation of Randle cycle regulation discussed above and the need for high rates of glycolysis to sustain tumor growth at its highest levels (2,35,36).”
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“…it was hypothesized that Que could affect the viability of SHI-1 cells by inhibiting glycolysis activity. c-Myc is a key regulator of glycolysis [23] , which can directly affect the transcription of GLUT1, HK2, PKM2, and LDHA genes [ 24 , 25 ] , and plays an important role in cancer cell…”
Additional file 1 of Targeting MYC-enhanced glycolysis for the treatment of small cell lung cancer
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“These results led us to conclude that RBM23 plays a role in regulating c-Myc in colon cancer. c-Myc is a master regulator of cellular metabolism, particularly glycolysis [53–55].”
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Lipid Metabolism, Lipogenesis, and Resistance to Third Generation EGFR‐TKIs
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“Although it has been proposed that MYC amplifies transcription on a global scale, the most highly de-regulated gene targets tend to be those involved in specific growth-related functions such as cell cycle control, metabolism, ribosomal biogenesis, translation and mRNA splicing (2, 4, 6, 10-12).”
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“…is the transcription factor c-Myc, which regulates mitochondrial biogenesis, expression of the nuclear-encoded mitochondrial genes [62], and mitochondrial dynamics [63], and is also involved in the regulation of metabolic processes, including glycolysis and oxidative phosphorylation [64].”
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“MYC also regulates glycolytic enzymes that regenerate NAD + [34], suggesting a role in NAD redox homeostasis.”
Kudo, M., van der Ent, M. A., Ballard, M., Gorman, J. A., & Cleuren, A. C. A. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.09.23.753727
“This might be particularly relevant given the central role of MYC in coordinating glycolytic and biosynthesis programs, 49,50 as it suggests that IL-6 promotes a more persistent metabolic adaptation than LPS, potentially contributing to the prolonged effects observed on barrier function.”
c-Myc Links TGF-β Signaling to Metabolic Control of HIV Reactivation in OM10.1 Cells
Harrison-Gleason, J., Kim, J., & Martinelli, E. (2026) · Microorganisms · doi:10.3390/microorganisms14102368
“…study was the identification of c-Myc as a potential mediator linking TGF-β signaling to this metabolically quiescent state. c-Myc c-Myc is a central regulator of cellular growth and metabolism, coordinating glycolysis, oxidative phosphorylation, glutaminolysis and other anabolic programs [51,56].”
Metadata
- Authors
- Goetzman, E. S., & Prochownik, E. V.
- Affiliations
- Children's Hospital of Pittsburgh (US)
- University of Pittsburgh (US)
- Corresponding author
- Prochownik, Edward V.
- Venue
- Frontiers in Endocrinology
- Publisher
- Frontiers Media SA
- Published
- 2018-04-12
- Volume
- 9
- Pages
- 129-129
- ISSN
- 1664-2392 (ISSN-L)
- PMC
- PMC5907532
- OpenAlex
- W2797261189
- Cited by
- 199
- References
- 309
- Citations by year
- 2026: 14 · 2025: 20 · 2024: 28 · 2023: 23 · 2022: 33 · 2021: 26 · 2020: 32 · 2019: 17 · 2018: 6
- FWCI
- 2.10
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Frontiers in Endocrinology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health (CA174713, DK090242)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Keywords
- c-Myc, cancer metabolism, glycolysis, oxidative phosphorylation, glutaminolysis, fatty acid metabolism, tumor cell proliferation, metabolic reprogramming, tumor evolution, metabolic plasticity
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