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

Dear Colleagues,

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

At the same time, Warburg hypothesized that the 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 through apoptosis or necrosis, and 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, with some of these data specifically indicating that the modulation of mitochondrial respiration may induce an arrest of cancer cell proliferation and differentiation (pseudodifferentiation) and/or death, suggesting that the 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 the pathophysiology and therapy of the so-called cancer stem cells.

At last, but not least, genomic, proteomic, and transcriptomic studies seem to show a lot of mitochondria in the modulation of the peculiar cancer cell microenvironment and metastasis dissemination.

At present, the relationship between mitochondria and cancer is quite tangled, and even if some aspects underlining the potential translational applications of intriguing pathophysiological links begin to emerge, mitochondria are not innocent bystanders in cancer progression, having various important pathogenetic roles in fundamental diagnostic, prognostic, and therapeutic implications.

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

Prof. Dr. 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