The Role for Myc in Coordinating Glycolysis, Oxidative Phosphorylation, Glutaminolysis, and Fatty Acid Metabolism in Normal and Neoplastic Tissues.
Level 5 - mechanism / opinion, no new human data
Narrative review outlining mechanistic frameworks without primary empirical data
PubMed 29706933 · doi:10.3389/fendo.2018.00129
What was done
This is a narrative review presenting a conceptual framework of cellular metabolism in normal quiescent cells versus rapidly proliferating and neoplastic tissues. The authors summarize the biochemical pathways—specifically glycolysis, oxidative phosphorylation, glutaminolysis, and fatty acid metabolism—regulated by the c-Myc (Myc) oncoprotein, and discuss potential therapeutic targeting strategies based on transformed metabolic pathways.
What was found
The abstract reports conceptual conclusions rather than empirical or quantitative data (no numbers, effect sizes, or statistical metrics are provided). It describes that cancer cells and normal cells share the same underlying metabolic pathways; however, quiescent cells direct metabolic intermediates toward organelle maintenance and homeostasis, whereas cancer cells under Myc influence divert these intermediates into anabolic pathways to support unremitting proliferation and metabolic plasticity under nutrient- and oxygen-deprived conditions.
Why it matters
The review frames Myc-driven metabolic reprogramming as an exaggerated, persistent version of normal proliferation programs rather than an entirely novel or mitochondrial-defective metabolic state. This clarifies the mechanistic rationale for targeting metabolic vulnerabilities shared across diverse transformed tissues.
Limits
The abstract provides no primary clinical or experimental data, quantitative measurements, systematic search methodology, or study inclusion criteria. Findings represent expert narrative synthesis and theoretical modeling of molecular mechanisms rather than tested therapeutic outcomes in human populations.
Cited by
- contradicts Every major cancer has damaged mitochondria and insufficient oxidative phosphorylation, rendering them dependent on fermentation of glucose and glutamine.