Warburg effect

The Warburg effect is the observation that most cancer cells release energy predominantly through a process of aerobic glycolysis consisting of a high level of glucose uptake and glycolysis followed by lactic acid fermentation taking place in the cytosol, not the mitochondria, even in the presence of abundant oxygen.

Most cancer cells do not release energy through the citric acid cycle and oxidative phosphorylation in the mitochondria as observed in normal cells.

Fermentation produces adenosine triphosphate (ATP) only in low yield compared to the citric acid cycle and oxidative phosphorylation of aerobic respiration, it allows proliferating cells to convert nutrients such as glucose and glutamine more efficiently into biomass by avoiding unnecessary catabolic oxidation of such nutrients into carbon dioxide, preserving carbon-carbon bonds and promoting anabolism.

The increased glucose consumption by cancer cells from the Warburg effect is the basis for tumor detection in a PET scan, in which an injected radioactive glucose analog is detected at higher concentrations in malignant cancers than in other tissues.

The deprivation of glucose and oxygen in tumor cells leads to a lack of energy, resulting in cell death. 

Cancer cells tend to use fermentation for obtaining energy even in aerobic conditions -aerobic glycolysis.

Dysfunctional mitochondria may be the cause of the higher rate of glycolysis seen in tumor cells, as well as a predominant cause of cancer development.

Mutations in oncogenes and tumor suppressor genes are thought to be responsible for malignant transformation, and the Warburg effect is considered to be a result of these mutations rather than a cause.

Fermentation favors cell proliferation.

The Warburg effect is associated with glucose uptake and use, as this ties into how mitochondrial activity is regulated. 

Tumor cells exhibit increased rates of glycolysis which can be explained with mitochondrial damage.

The increase in nutrient uptake by cancer cells as a treatment target by exploitation of a critical proliferation tool in cancer.

Nutrient use is dramatically altered when cells receive signals to proliferate, with metabolic changes enabling cells to meet the large biosynthetic demands associated with cell growth and division. 

Metabolic reprogramming in cancer is largely due to the oncogenic activation of signal transduction pathways and transcription factors.

Epigenetic mechanisms also contribute to the regulation of metabolic gene expression in cancer.

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