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 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.
“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]
Transcription factors c-Myc and ATF4 are two master-regulators of glycolysis, respiration, and one-carbon metabolism.
“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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Analysis of gene expression during myc oncogene-induced lymphomagenesis in the bursa of Fabricius
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The transport of glutamine into mammalian cells
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The metabolic signature of macrophage responses
Viola, A., Munari, F., Sánchez-Rodríguez, R., Scolaro, T., & Castegna, A. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.01462 · Cited by 2,021 · see citing works
“Free fatty acids are subsequently transported into mitochondria, where they are converted by the FAO pathway into different products that continuously replenish the TCA cycle with acetylcoenzyme A, or the ETC through the generation of NADH and FADH2 (148).”
BackgroundInfluentialRegulation and metabolic functions of mTORC1 and mTORC2.
Szwed, A., Kim, E., & Jacinto, E. (2021) · Physiological Reviews · doi:10.1152/physrev.00026.2020 · Cited by 723 · see citing works
Signaling pathways and targeted therapies for psoriasis
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BackgroundThe ERK and JNK pathways in the regulation of metabolic reprogramming
Papa, S., Choy, P. M., & Bubici, C. (2018) · Oncogene · doi:10.1038/s41388-018-0582-8 · Cited by 381 · see citing works
Targeting multiple signaling pathways: the new approach to acute myeloid leukemia therapy
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Regulation of Tumor Initiation by the Mitochondrial Pyruvate Carrier
Bensard, C., Wisidagama, D. R., Olson, K. A., Berg, J. A., Krah, N. M., Schell, J. C., Nowinski, S. M., Fogarty, S., Bott, A. J., Wei, P., et al. (2019) · Cell Metabolism · doi:10.1016/j.cmet.2019.11.002 · Cited by 170 · see citing works
“Carbohydrate and fatty acid oxidation have a welldescribed antagonistic relationship and it has been repeatedly observed that loss of MPC activity (and carbohydrate oxidation) leads to increased fatty acid oxidation and vice versa (Goetzman and Prochownik, 2018; Hue and Taegtmeyer, 2009; Schell et al., 2017).”
BackgroundTherapeutic targeting of glutaminolysis as an essential strategy to combat cancer
Matés, J. M., Paola, F. J. D., Campos-Sandoval, J. A., Mazurek, S., & Márquez, J. (2019) · Seminars in Cell and Developmental Biology · doi:10.1016/j.semcdb.2019.05.012 · Cited by 164 · see citing works
The Metabolic Fates of Pyruvate in Normal and Neoplastic Cells
Prochownik, E. V., & Wang, H. (2021) · Cells · doi:10.3390/cells10040762 · Cited by 145 · see citing works
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Metabolic Fitness and Plasticity in Cancer Progression
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Samec, M., Líšková, A., Koklesová, L., Samuel, S. M., Zhai, K., Buhrmann, C., Varghese, E., Abotaleb, M., Qaradakhi, T., Zulli, A., et al. (2020) · The EPMA Journal · doi:10.1007/s13167-020-00217-y · Cited by 131 · see citing works
“In addition, it has been suggested that c-Myc and HIF-1 cooperate in the regulation of glycolysis [43].”
BackgroundMolecular and Cellular Mechanisms of Propolis and Its Polyphenolic Compounds against Cancer
Oršolić, N., & Jembrek, M. J. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms231810479 · Cited by 132 · see citing works
Cai, J., Chen, Z., Wang, J., Wang, J., Chen, X., Liang, L., Huang, M., Zhang, Z., & Zuo, X. (2019) · Cell Death and Disease · doi:10.1038/s41419-019-1814-8 · Cited by 124 · see citing works
Flavonoids Targeting HIF-1: Implications on Cancer Metabolism
Samec, M., Líšková, A., Koklesová, L., Meršaková, S., Strnádel, J., Kajo, K., Péč, M. J., Zhai, K., Šmejkal, K., Mirzaei, S., et al. (2021) · Cancers · doi:10.3390/cancers13010130 · Cited by 114 · see citing works
The role of Wnt signaling pathway in tumor metabolic reprogramming
Mo, Y., Wang, Y., Zhang, L., Yang, L., Zhou, M., Li, X., Li, Y., Li, G., Zeng, Z., Xiong, W., et al. (2019) · Journal of Cancer · doi:10.7150/jca.31166 · Cited by 106 · see citing works
“Thereby promoting the glycolysis, nucleotide and fatty acid synthesis in tumor cells, providing tumor cells with the substances and energy required for proliferation [91-94].”
BackgroundLong non-coding RNAs involved in cancer metabolic reprogramming
Liu, H., Luo, J., Luan, S., He, C., & Li, Z. (2018) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-018-2946-1 · Cited by 98 · see citing works
Targeting O-GlcNAcylation to develop novel therapeutics
Zhu, Y., & Hart, G. W. (2020) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2020.100885 · Cited by 92 · see citing works
Yuan, M., Tu, B., Li, H., Pang, H., Zhang, N., Fan, M., Bai, J., Wang, W., Shu, Z., DuFort, C. C., et al. (2022) · Nature Cancer · doi:10.1038/s43018-022-00426-6 · Cited by 96 · see citing works
The Regulation and Function of the L-Type Amino Acid Transporter 1 (LAT1) in Cancer
Salisbury, T. B., & Arthur, S. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19082373 · Cited by 91 · see citing works
Mossenta, M., Busato, D., Bo, M. D., & Toffoli, G. (2020) · Cancers · doi:10.3390/cancers12061668 · Cited by 90 · see citing works
Papaccio, F., García-Micó, B., Gimeno-Valiente, F., Cabeza-Segura, M., Gambardella, V., Gutiérrez-Bravo, M. F., Alfaro‐Cervelló, C., Martínez‐Ciarpaglini, C., Rentero-Garrido, P., Zúñiga, S., et al. (2023) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-022-02591-z · Cited by 88 · see citing works
“GSEA analysis showed that RTO7 is enriched in MYC targets hallmarks, fatty acids and lipid biosynthesis (which together are a consequence of MYC activation [56]) and unfolded protein response (Fig.”
BackgroundOh, C. J., Kim, M., Lee, J.-M., Kim, D. H., Kim, I., Park, S., Kim, Y., Lee, K., Lee, S., Lim, C. W., et al. (2023) · Kidney International · doi:10.1016/j.kint.2023.06.022 · Cited by 84 · see citing works
Викторович, П. Д., Makhnovskii, P. A., Shagimardanova, E. I., Gazizova, G. R., Lysenko, E. A., Gusev, O., & Виноградова, О. Л. (2019) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00449.2018 · Cited by 80 · see citing works
“Cellular studies show that MYC regulates lipid metabolism, nucleotide synthesis, angiogenesis, expression of the mitochondrial transcription factor TFAM, and mitochondrial biogenesis (1, 8, 11); also, chronic electrostimulation increases the MYC content of rat muscle and activates mitochondrial biogenesis (19).”
BackgroundBae, S., Park, P. S. U., Lee, Y., Mun, S. H., Γιαννοπούλου, Ε., Fujii, T., Lee, K. P., Violante, S. N., Cross, J. R., & Park‐Min, K. (2021) · Cell Reports · doi:10.1016/j.celrep.2021.109264 · Cited by 79 · see citing works
“The link between MYC and altered cellular metabolism has been previously established in cancer and T cells (Dang et al., 2009; Goetzman and Prochownik, 2018).”
Control of cell metabolism by the epidermal growth factor receptor
Orofiamma, L. A., Vural, D., & Antonescu, C. N. (2022) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2022.119359 · Cited by 69 · see citing works
Reiter, R. J., Sharma, R., & Rosales‐Corral, S. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22020764 · Cited by 68 · see citing works
Robb, J. L., Hammad, N. A., Potter, P. G. W., Chilton, J. K., Beall, C., & Ellacott, K. L. J. (2020) · Glia · doi:10.1002/glia.23835 · Cited by 66 · see citing works
“NF-κB signaling mediates increases in expression of c-Myc, a transcriptional regulator of glycolytic genes (Goetzman & Prochownik, 2018; La Rosa, Pierce, & Sonenshein, 1994), in fibroblasts and of hexokinase II in sarcoma cells (Londhe et al., 2018).”
BackgroundThe spectrum of macrophage activation by immunometabolism
Kang, S., & Kumanogoh, A. (2020) · International Immunology · doi:10.1093/intimm/dxaa017 · Cited by 63 · see citing works
Linking Metabolic Reprogramming, Plasticity and Tumor Progression
Shuvalov, O., Daks, A., Fedorova, O., Petukhov, A., & Barlev, N. (2021) · Cancers · doi:10.3390/cancers13040762 · Cited by 63 · see citing works
Targeting MYC-enhanced glycolysis for the treatment of small cell lung cancer
Cargill, K. R., Stewart, C. A., Park, E. M., Ramkumar, K., Gay, C. M., Cardnell, R. J., Wang, Q., Diao, L., Shen, L., Fan, Y.-H., et al. (2021) · Cancer & Metabolism · doi:10.1186/s40170-021-00270-9 · Cited by 62 · see citing works
Misund, K., Bruinink, D. H. O., Coward, E., Hoogenboezem, R. M., Rustad, E. H., Sanders, M. A., Rye, M. B., Sponaas, A., van der Holt, B., Zweegman, S., et al. (2022) · Leukemia · doi:10.1038/s41375-022-01597-y · Cited by 56 · see citing works
“MYC is an important regulator of metabolic pathways, including glycolysis and oxidative phosphorylation (reviewed in [49]).”
BackgroundSen, K., Pati, R., Jha, A., Mishra, G. P., Prusty, S., Chaudhary, S., Swetalika, S., Podder, S., Sen, A., Swain, M., et al. (2022) · Redox Biology · doi:10.1016/j.redox.2022.102575 · Cited by 56 · see citing works
pH gradient reversal fuels cancer progression
Zheng, T., Jäättelä, M., & Liu, B. (2020) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2020.105796 · Cited by 55 · see citing works
Glycolysis and Fatty Acid Oxidation Inhibition Improves Survival in Glioblastoma
McKelvey, K. J., Wilson, E., Short, S. C., Melcher, A. A., Biggs, M. T., Diakos, C. I., & Howell, V. M. (2021) · Frontiers in Oncology · doi:10.3389/fonc.2021.633210 · Cited by 53 · see citing works
“Glucose metabolism and reactive oxygen species (ROS) are bidirectionally linked, and cancer cells are metabolically adaptive to the changing oxygen and nutrient microenvironment (19).”
BackgroundTargeting Myc-driven stress addiction in colorectal cancer
Saeed, H., Leibowitz, B. J., Zhang, L., & Yu, J. (2023) · Drug Resistance Updates · doi:10.1016/j.drup.2023.100963 · Cited by 53 · see citing works
Inflammescent CX3CR1+CD57+CD8+ T cells are generated and expanded by IL-15
Morris, S. R., Chen, B., Mudd, J. C., Panigrahi, S., Shive, C. L., Sieg, S. F., Cameron, C., Zidar, D. A., Funderburg, N., Younes, S., et al. (2020) · JCI Insight · doi:10.1172/jci.insight.132963 · Cited by 52 · see citing works
“IL-15 likely elicits these effects, at least in part, through its upregulation of c-myc, since c-myc activity is strongly linked to cell proliferation (46), mitochondrial biogenesis (47), and cell metabolism (48), and c-myc has been shown to be important for IL-15–mediated homeostatic proliferation of CD8+ Tmem (31).”
BackgroundSong, X., Chang, S., Seminario‐Vidal, L., Pulido, Á. D. M., Tordesillas, L., Song, X., Reed, R. A., Harkins, A., Whiddon, S., Nguyen, J. V., et al. (2022) · Cancer Discovery · doi:10.1158/2159-8290.cd-21-1207 · Cited by 49 · see citing works
Metabolomics and the Multi-Omics View of Cancer
Wishart, D. S. (2022) · Metabolites · doi:10.3390/metabo12020154 · Cited by 51 · see citing works
CD47 and thrombospondin-1 regulation of mitochondria, metabolism, and diabetes
Roberts, D. D., & Isenberg, J. S. (2021) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00175.2021 · Cited by 48 · see citing works
Beyond the Warburg Effect: N-Myc Contributes to Metabolic Reprogramming in Cancer Cells
Yoshida, G. J. (2020) · Frontiers in Oncology · doi:10.3389/fonc.2020.00791 · Cited by 46 · see citing works
Kim, D., Kim, G., Yu, R., Lee, J., Kim, S., Gleason, M. R., Qiu, K., Montauti, E. I., Wang, L. L., Fang, D., et al. (2024) · Immunity · doi:10.1016/j.immuni.2024.08.008 · Cited by 48 · see citing works
Wang, H., Dolezal, J. M., Kulkarni, S., Lu, J. L., Mandel, J. A., Jackson, L. E., Alencastro, F., Duncan, A. W., & Prochownik, E. V. (2018) · Journal of Biological Chemistry · doi:10.1074/jbc.ra118.004099 · Cited by 46 · see citing works
Self-citationMYC—an emerging player in mitochondrial diseases
Purhonen, J., Klefström, J. T., & Kallijärvi, J. (2023) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2023.1257651 · Cited by 40 · see citing works
“The Warburg effect is now known to occur in both rapidly proliferating normal cells and cancer cells without any impairment in OXPHOS (Senyilmaz and Teleman, 2015; Goetzman and Prochownik, 2018; Vaupel and Multhoff, 2021).”
BackgroundInfluentialThe Integration of Metabolomics with Other Omics: Insights into Understanding Prostate Cancer
Resurreccion, E. P., & Fong, K.-W. (2022) · Metabolites · doi:10.3390/metabo12060488 · Cited by 44 · see citing works
How could we forget immunometabolism in SARS-CoV2 infection or COVID-19?
Kumar, V. (2020) · International Reviews of Immunology · doi:10.1080/08830185.2020.1840567 · Cited by 39 · see citing works
Fame, R. M., Shannon, M. L., Chau, K. F., Head, J. P., & Lehtinen, M. K. (2019) · Development · doi:10.1242/dev.182857 · Cited by 38 · see citing works
“Because MYC targets are also involved in many mitochondrial and hypoxia-related processes (Doe et al., 2012; Goetzman and Prochownik, 2018; Morrish and Hockenbery, 2014), we investigated mitochondria after experimentally extending the time and level of MYC expression in neuroepithelial progenitors by expressing a huma…”
BackgroundInfluentialMyc‐dependent endothelial proliferation is controlled by phosphotyrosine 1212 in VEGF receptor‐2
Testini, C., Smith, R., Jin, Y., Martinsson, P., Sun, Y., Hedlund, M., Sáinz‐Jaspeado, M., Shibuya, M., Hellström, M., & Claesson, L. (2019) · EMBO Reports · doi:10.15252/embr.201947845 · Cited by 37 · see citing works
“ERK1/2 and Akt pathways positively and negatively regulate the expression of c-Myc [20,21], a transcription factor that controls expression of a broad set of genes involved in cell cycle progression, cell proliferation, apoptosis, and cell metabolism [20,22].”
Qiao, X., Ma, J., Knight, T. E., Su, Y., Edwards, H. J., Polin, L., Li, J., Kushner, J., Dzinic, S. H., White, K., et al. (2021) · Blood Cancer Journal · doi:10.1038/s41408-021-00502-7 · Cited by 36 · see citing works
Metabolic Strategies for Inhibiting Cancer Development
Icard, P., Loi, M., Wu, Z., Ginguay, A., Lincet, H., Robin, E., Coquerel, A., Berzan, D., Fournel, L., & Alifano, M. (2020) · Advances in Nutrition · doi:10.1093/advances/nmaa174 · Cited by 36 · see citing works
“c-MYC (55, 56) Amplification ↑GLUT1 (51) ↑LDH-A ↑SHMT2 ↑HK2 (51) ↑PFK1 ↑MCT4 ↑OXPHOS Stimulation of glucose transport and glycolysis”
Zhang, Y., Wang, Y., Li, Y., Huang, C., Xiao, X., Zhong, Z., Tang, J., Lu, H., Tang, Y., & Yang, J. (2022) · Biochemical Pharmacology · doi:10.1016/j.bcp.2022.114941 · Cited by 35 · see citing works
Phosphoenolpyruvate from Glycolysis and PEPCK Regulate Cancer Cell Fate by Altering Cytosolic Ca2+
Moreno-Felici, J., Hyroššová, P., Aragó, M., Rodríguez‐Arévalo, S., García-Rovés, P. M., Escolano, C., & Perales, J. C. (2019) · Cells · doi:10.3390/cells9010018 · Cited by 35 · see citing works
BCG Vaccinations Upregulate Myc, a Central Switch for Improved Glucose Metabolism in Diabetes
Kühtreiber, W. M., Takahashi, H., Keefe, R. C., Song, Y., Tran, L., Luck, T. G., Shpilsky, G. F., Moore, L., Sinton, S. M., Graham, J. C., et al. (2020) · iScience · doi:10.1016/j.isci.2020.101085 · Cited by 35 · see citing works
“The data pull together many of the sugar regulation pathways under Myc’s regulatory control: glycolysis, glutaminolysis, polyamine synthesis, and the HIF-1a/mTOR pathway (Goetzman and Prochownik, 2018; Rathmell, 2011; Wang et al., 2011).”
BackgroundChemoresistance: The hidden barrier in cancer treatment
Dhiman, V. K., Kumari, M., & Singh, D. (2025) · Cancer Pathogenesis and Therapy · doi:10.1016/j.cpt.2025.07.001 · Cited by 35 · see citing works
“67,68 Cancer-associated fibroblasts (CAFs) also undergo metabolic reprogramming, adopting aerobic glycolysis and exporting metabolic like lactate and ketone bodies to fuel tumor cells.”
Rezinciuc, S., Bezavada, L., Bahadoran, A., Duan, S., Wang, R., López‐Ferrer, D., Zink, E. E., Finklestein, D., Green, D. R., Paša‐Tolić, L., et al. (2020) · PLoS Pathogens · doi:10.1371/journal.ppat.1008957 · Cited by 34 · see citing works
“c-Myc is considered a master regulator of cancer metabolism, and metabolic reprogramming by c-Myc is thought to allow cancer and activated immune cells to sustain supplies of anabolic building blocks while generating energy for their assembly [14, 63, 64, 67, 71].”
BackgroundTargeting Pin1 for Modulation of Cell Motility and Cancer Therapy
Chuang, H.-H., Zhen, Y., Tsai, Y.-C., Chuang, C., Huang, M., Hsiao, M., & Yang, C. (2021) · Biomedicines · doi:10.3390/biomedicines9040359 · Cited by 33 · see citing works
Normal and Neoplastic Growth Suppression by the Extended Myc Network
Wang, H., & Prochownik, E. (2022) · Cells · doi:10.3390/cells11040747 · Cited by 31 · see citing works
Self-citationSerra, M., Matteo, M. D., Serneels, J., Pal, R. R., Cafarello, S. T., Lanza, M., Sànchez‐Martìn, C., Evert, M., Castegna, A., Calvisi, D. F., et al. (2022) · Cellular and Molecular Gastroenterology and Hepatology · doi:10.1016/j.jcmgh.2022.06.003 · Cited by 31 · see citing works
“Indeed, it ensures the continuous generation of NADþ to serve as an electron acceptor during glucose oxidation.(7) Thus, lactate should be considered a critical oncometabolite in the metabolic reprogramming of cancer and LDH as a suitable therapeutic target for cancer treatment.”
BackgroundInfluentialGonçalves, M., Aiello, A., Rodríguez-Pérez, M., Accardi, G., Burgos‐Ramos, E., & Silva, P. (2024) · Nutrients · doi:10.3390/nu16060818 · Cited by 31 · see citing works
“These cancer cells start relying on oxidative phosphorylation and aerobic glycolysis, with both processes being upregulated to guarantee the efficient production of ATP and the consequent rapid accumulation of biomass and rate of proliferation [52].”
BackgroundDual Inhibition of CDK4/6 and PI3K/AKT/mTOR Signaling Impairs Energy Metabolism in MPM Cancer Cells
Bonelli, M. A., Terenziani, R., Zoppi, S., Fumarola, C., Monica, S. L., Cretella, D., Alfieri, R. R., Cavazzoni, A., Digiacomo, G., Galetti, M., et al. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21145165 · Cited by 31 · see citing works
The O-GlcNAcylation and its promotion to hepatocellular carcinoma
Zhang, J., Xun, M., Li, C., & Chen, Y. (2022) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2022.188806 · Cited by 31 · see citing works
Liu, S., Qiao, X., Wu, S., Gai, Y., Su, Y., Edwards, H. J., Wang, Y., Lin, H., Taub, J. W., Wang, G., et al. (2022) · APOPTOSIS · doi:10.1007/s10495-022-01756-7 · Cited by 30 · see citing works
Wang, H., Lu, J. L., Stevens, T., Roberts, A., Mandel, J. A., Avula, R., Ma, B., Wu, Y. L., Wang, J., Land, C. V., et al. (2023) · Cell Reports · doi:10.1016/j.celrep.2023.112830 · Cited by 28 · see citing works
“14,71,78,87 The Glut1 glucose transporter, whose gene is a Myc target, 78 and Glut4 87 were regulated oppositely in 5-month-old MycKO livers, whereas Glut2 did not change.”
Self-citationJonsson, M., Fjeldbo, C. S., Holm, R., Stokke, T., Kristensen, G. B., & Lyng, H. (2019) · Neoplasia · doi:10.1016/j.neo.2019.01.002 · Cited by 29 · see citing works
“MYC has been shown to drive proliferation of tumor cells through a positive effect on both glycolysis and OXPHOS and regulation of fatty acid metabolism [28].”
BackgroundDesmet, K. L. J., Marei, W. F. A., Richard, C., Sprangers, K., Beemster, G. T. S., Meysman, P., Laukens, K., Declerck, K., Berghe, W. V., Bols, P. E. J., et al. (2019) · Human Reproduction · doi:10.1093/humrep/dez248 · Cited by 28 · see citing works
Wahab, A. H. A. A., Effat, H., Mahrous, E. A., Ali, M. A., & Al‐Shafie, T. A. (2020) · Nutrition and Cancer · doi:10.1080/01635581.2020.1783329 · Cited by 28 · see citing works
The many lives of Myc in the pancreatic β-cell
Rosselot, C., Baumel-Alterzon, S., Li, Y., Brill, G., Lambertini, L., Katz, L. S., Lu, G., Garcı́a-Ocaña, A., & Scott, D. K. (2020) · Journal of Biological Chemistry · doi:10.1074/jbc.rev120.011149 · Cited by 30 · see citing works
“Myc participates in the stimulation of global protein expression for the purpose of increasing cell mass before cell division, through the activation of RNA polymerase I, II, and III and of genes that take part in ribosome biosynthesis, ribosome structure, and tRNA and rRNA synthesis (47, 49).”
BackgroundPatient-Derived Mutant Forms of NFE2L2/NRF2 Drive Aggressive Murine Hepatoblastomas
Wang, H., Lu, J. L., Mandel, J. A., Zhang, W., Schwalbe, M., Gorka, J. E., Liu, Y., Marburger, B., Wang, J., Ranganathan, S., et al. (2021) · Cellular and Molecular Gastroenterology and Hepatology · doi:10.1016/j.jcmgh.2021.02.004 · Cited by 27 · see citing works
Self-citationLDHB Overexpression Can Partially Overcome T Cell Inhibition by Lactic Acid
Decking, S.-M., Bruß, C., Babl, N., Bittner, S., Klobuch, S., Thomas, S., Feuerer, M., Hoffmann, P., Dettmer, K., Oefner, P. J., et al. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23115970 · Cited by 27 · see citing works
Targeting the Metabolic Paradigms in Cancer and Diabetes
Bosso, M., Haddad, D., Madhoun, A. S. A., & Al‐Mulla, F. (2024) · Biomedicines · doi:10.3390/biomedicines12010211 · Cited by 26 · see citing works
Ruan, J. J., Yu, Y., Hou, W., Chen, Z., Fang, J., Zhang, J., Ni, M., Li, D., Lu, S., Rui, J., et al. (2019) · ACS Pharmacology & Translational Science · doi:10.1021/acsptsci.8b00047 · Cited by 27 · see citing works
Peroxynitrite promotes serine-62 phosphorylation-dependent stabilization of the oncoprotein c-Myc
Raman, D., Chong, S. J. F., Iskandar, K. B., Hirpara, J. L., & Pervaiz, S. (2020) · Redox Biology · doi:10.1016/j.redox.2020.101587 · Cited by 25 · see citing works
Li, L., Peng, G., Liu, X., Zhang, Y., Han, H., & Liu, Z. (2020) · iScience · doi:10.1016/j.isci.2020.101684 · Cited by 26 · see citing works
“It is known that c-myc regulates glutaminolysis by controlling GLS-1 expression (Gao et al., 2009; Goetzman and Prochownik, 2018; Wise et al., 2008).”
BackgroundCTPS and IMPDH form cytoophidia in developmental thymocytes
Peng, M., Chang, C., Liu, J., & Sung, L. (2021) · Experimental Cell Research · doi:10.1016/j.yexcr.2021.112662 · Cited by 26 · see citing works
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“The contribution of MYC to metabolism in normal and neoplastic tissues is extensive [43, 44].”
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“Activation of p53 is also linked to metabolic rewiring ( 51 ), in part by repressing Myc ( 52 ), a proto-oncogene that codes for Myc transcription factor and is linked to the up-regulation of the glycolytic pathway in cancer cells ( 53 ).”
The hepatic microenvironment and regulatory T cells
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“This alteration tends to provide convenient materials and fast energy supplies for cancer growth and proliferation.(37)”
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Propionic acid induces alterations in mitochondrial morphology and dynamics in SH-SY5Y cells
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Coordinated Cross-Talk Between the Myc and Mlx Networks in Liver Regeneration and Neoplasia
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“Through regulation of phosphorylation, TSP1-CD47 signaling destabilized cMyc [70], which plays significant roles in regulating glycolysis, fatty acid homeostasis, and metabolism, suggesting that TSP1-CD47 signaling negatively controls cellular metabolism by decreasing the expression of cMyc [71].”
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“In many tumors, this is coordinated by the oncoprotein c-Myc (44).”
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“Interestingly, Myc is also able to transfer glucose produced via aerobic metabolism through the TCA cycle to the anaerobic glycolysis process (33).”
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Multi-omics data integration approach identifies potential biomarkers for Prostate cancerPreprint
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Pathobiology and Therapeutic Relevance of GSK-3 in Chronic Hematological Malignancies
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N-acetylcysteine overcomes NF1 loss-driven resistance to PI3Kα inhibition in breast cancer
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“We did not investigate mitochondrial function, fusion, and fission, which could be affected by enhanced MAPK and/or MYC activity.(47) Interestingly, NF1 KO cells were more sensitive to pharmacological MYC inhibition than CTRL cells, and we observed an additive effect of MYC inhibition in combination with PI3Ka inhibit…”
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- 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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