Mitochondria in Cancer: A Neglected Functional Reprogramming with Fundamental Pathophysiological Implications

Dear Colleagues,

At the beginning of the twentieth century, Otto Warburg demonstrated that cancer cells have a peculiar metabolism. These cells preferentially utilize glycolysis for energetic and anabolic purposes, producing large quantities of lactic acid. He defined this unusual metabolism “aerobic glycolysis”.

At the same time, Warburg hypothesized that a disruption of mitochondrial activities played a precise pathogenic role in cancer.

Over time, however, many studies have shown that mitochondria play a fundamental role in cell death by apoptosis or necrosis. Moreover, metabolic enzymes of the Krebs cycle have also recently been recognized as oncosuppressors. Recently, a series of studies were undertaken to re-evaluate the role of oxidative mitochondrial metabolism in cancer cell growth and progression. Some of these data specifically indicate that modulation of mitochondrial respiration may induce an arrest of cancer cell proliferation and differentiation (pseudodifferentiation) and/or death, suggesting that iatrogenic manipulation of some mitochondrial activities may induce anticancer effects. Moreover, studying the role of mitochondria, above all in terms of ROS and RNOS signaling, in cancer cell dedifferentiation/differentiation processes may allow further insight into the peculiar cancer cell plasticity and on pathophysiology and therapy of so-called cancer stem cells. At present, the relationship between mitochondria and cancer is quite difficult. It is only possible to stress some aspects that underline the potential translational applications of intriguing pathophysiological links. Mitochondria are not innocent bystanders in cancer progression. They have various important pathogenetic roles with fundamental diagnostic, prognostic, and therapeutic implications.

Last but not least, elucidating the relationship between cancer cell mitochondria and cellular differentiation state is fundamental not only for the field of oncology but also for the physiology and pathophysiology of stem cells in general and cancer stem cells in particular.

Prof. Roberto Scatena
Guest Editor

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• electron respiratory chain
• cell signaling
• cancer cell plasticity
• cancer cell differentiation
• mitochondria
• free radical species
• biomarkers
• oncotherapy