Reexamining cancer metabolism: lactate production for carcinogenesis could be the purpose and explanation of the Warburg Effect
Level 5 - mechanism / opinion, no new human data
Mechanism-based reasoning and theoretical hypothesis paper with no empirical human data.
OpenAlex W2562182278 · doi:10.1093/carcin/bgw127
What was done
This conceptual paper applied principles from exercise physiology and metabolic signaling to formulate a mechanistic hypothesis regarding the role of lactate in cancer. It outlines a theoretical framework ('lactagenesis') to explain the functional purpose of the Warburg effect in driving carcinogenesis.
What was found
The abstract reports a conceptual model and contains no quantitative experimental numbers or empirical data. The authors propose a five-step sequence in lactagenic cancer cells: increased glucose uptake, increased glycolytic enzyme expression/activity, decreased mitochondrial function, increased lactate production and release, and upregulation of monocarboxylate transporters (MCT1 and MCT4). They hypothesize that lactate acts as an essential signaling molecule promoting angiogenesis, immune escape, cell migration, and metastasis.
Why it matters
The paper frames lactate not as an inert waste product of aerobic glycolysis, but as an active signaling driver of cancer progression, suggesting monocarboxylate transporters and lactate signaling pathways as key therapeutic targets.
Limits
The publication is purely theoretical and provides no original in vitro, in vivo, or clinical experimental data. Proposed mechanisms and therapeutic implications rely on theoretical synthesis rather than tested empirical interventions.
Cited by
- supports Otto Warburg was the first to define cancer as a metabolic disease.