Purpose of review
Recent evidence suggests that oxidative metabolism may have a key role in controlling cancer growth. This review will provide an overview of the evidence accumulated so far. More than 80 years ago, Otto Warburg suggested that impaired oxidative metabolism may cause malignant growth. This assumption, later known as Warburg's hypothesis, has been experimentally addressed for many decades. It employs multiple approaches including cell lines, implanted xenografts and other animal models, by biochemical methods to quantify glycolytic and mitochondrial fluxes and signaling pathways including the rates of intermediate metabolism, respiration and oxidative phosphorylation.
The hallmarks of cancer growth, increased glycolysis and lactate production in tumors, have raised attention recently due to novel observations suggesting a wide spectrum of oxidative phosphorylation deficits and decreased availability of ATP associated with malignancies and tumor cell expansion. The most recent findings suggest that forcing cancer cells into mitochondrial metabolism efficiently suppresses cancer growth, and that impaired mitochondrial respiration may even have a role in metastatic processes.
This review summarizes published evidence on the essential interaction of tumor growth and mitochondrial metabolism, implicating novel approaches for the prevention and treatment of malignant disease.