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Abstract
Cancer cells reprogram their metabolism to meet bioenergetics and biosynthetic demands. The first observation of metabolic reprogramming in cancer cells was made a century ago (“Warburg effect” or aerobic glycolysis), leading to the classical view that cancer metabolism relies on a glycolytic phenotype. There is now accumulating evidence that most cancers also rely on mitochondria to satisfy their metabolic needs. Indeed, the current view of cancer metabolism places mitochondria as key actors in all facets of cancer progression. Importantly, mitochondrial metabolism has become a very promising target in cancer therapy, including for refractory cancers such as Pancreatic Ductal AdenoCarcinoma (PDAC). In particular, mitochondrial oxidative phosphorylation (OXPHOS) is an important target in cancer therapy. Other therapeutic strategies include the targeting of glutamine and fatty acids metabolism, as well as the inhibition of the TriCarboxylic Acid (TCA) cycle intermediates. A better knowledge of how pancreatic cancer cells regulate mitochondrial metabolism will allow the identification of metabolic vulnerabilities and thus novel and more efficient therapeutic options for the benefit of each patient.
Highlights
Over the past decade, cancer researchers have turned their attention to the cellular organelle mitochondrion
The classical cancer energetic metabolism view describes the “Warburg effect” or aerobic glycolysis, characterized by high glycolytic rates observed in cancer cells even in the presence of oxygen, with a pathways related to energy production and biosynthesis (Figure 1)
The classical cancer energetic metabolism view describes the “Warburg effect” or aerobic glycolysis, characterized by high glycolytic rates observed in cancer cells even in the presence of consequent high amount of lactate production (Figure 1)
Summary
Cancer researchers have turned their attention to the cellular organelle mitochondrion. The outcome could be better with a therapeutic strategy that would include inhibitors of mitochondrial metabolism for the patients whose tumor depend on mitochondria for aggressiveness and resistance to therapy. We will first present the classical view of cancer metabolism over many decades, as well as an extensive analysis of several important aspects leading to the current view of cancer metabolism The latter is a comprehensive and integral approach to better understand cancer metabolism and metabolic dependencies, with a special focus on the specifics of pancreatic cancer. A better knowledge of how pancreatic cancer cells regulate their metabolism, in particular mitochondrial metabolism, will allow the design of novel and more efficient therapeutic options for the benefit of each patient
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