Abstract
Skin cancer is the most common type of cancer in the United States, with an increasing annual rate. Defining the mechanism of skin cancer malignancy and progression is the first step towards skin cancer prevention and therapy. “Warburg Effect” describes the preference of glycolysis and lactate fermentation rather than oxidative phosphorylation for energy production in cancer cells, which also present in non-melanoma and melanoma skin cancers. Mitochondrial metabolism is an important and necessary component in the functioning and maintenance of the organelle, and accumulating evidence suggests that dysfunction of mitochondrial metabolism plays a role in skin cancer. Recently, new progress has demonstrated the mechanisms of the mitochondrial metabolism-to-glycolysis switch in skin cancer development and how to target this metabolic switch for skin cancer prevention and therapy, which will be discussed in this review.
Highlights
In vertebrates, food is digested and supplied to cells mainly in the form of glucose
Mitochondrial oxygen consumption and intracellular Adenosine Triphosphate (ATP) levels are increased in arsenic-treated keratinocytes [15]. These results suggest that increased mitochondrial biogenesis may contribute to arsenic-induced skin cell proliferation
The results suggest that GIT-27/NO causes a dose-dependent reduction of mitochondrial respiration in treated A375 human melanoma cells [39]
Summary
Food is digested and supplied to cells mainly in the form of glucose. Many studies have demonstrated glycolysis as the main metabolic pathway in cancer cells [3,4,5,6]. A recent review on hypoxia nicely summarizes some current studies and speculates that the “Warburg Effect” provides a benefit to the tumor not by increasing glycolysis but by decreasing mitochondrial activity [8].
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