Cancer resistance and metastasis are maintained through oxidative phosphorylation.
Level 5 - mechanism / opinion, no new human data
Narrative review and mechanistic summary without systematic methodology
PubMed 38373691 · doi:10.1016/j.canlet.2024.216705
What was done
Narrative review summarizing recent literature on the upregulation of mitochondrial oxidative phosphorylation (OXPHOS) genes in chemoresistant tumors, cancer stem cells, and cell models, alongside reported associations between OXPHOS expression and post-chemotherapy survival.
What was found
The abstract reports no numerical values, effect sizes, or statistical metrics. It qualitatively reports that OXPHOS can operate concurrently with glycolysis during tumor evolution, that chemoresistant cells and cancer stem cells upregulate OXPHOS during metastasis, and that OXPHOS gene expression is inversely correlated with patient survival duration following chemotherapy.
Why it matters
It highlights tumor metabolic flexibility beyond the classical Warburg effect, suggesting OXPHOS as a potential therapeutic target in combination treatments for resistant malignancies.
Limits
This is a narrative review lacking a systematic search strategy or quantitative meta-analysis. The abstract provides no specific patient sample sizes, cancer types, quantitative risk estimates, or details on specific combination regimens. Described survival links represent observational correlations rather than prospective interventional findings.
Cited by
- contradicts All major cancers utilize fermentation driven by mitochondrial dysfunction to sustain uncontrolled tumor growth.