Abstract
Metabolism encompasses the biochemical processes that allow healthy cells to keep energy, redox balance and building blocks required for cell development, survival, and proliferation steady. Malignant cells are well-documented to reprogram their metabolism and energy production networks to support rapid proliferation and survival in harsh conditions via mutations in oncogenes and inactivation of tumor suppressor genes. Despite the histologic and genetic heterogeneity of tumors, a common set of metabolic pathways sustain the high proliferation rates observed in cancer cells. This review with a focus on lung cancer covers several fundamental principles of the disturbed glucose metabolism, such as the “Warburg” effect, the importance of the glycolysis and its branching pathways, the unanticipated gluconeogenesis and mitochondrial metabolism. Furthermore, we highlight our current understanding of the disturbed glucose metabolism and how this might result in the development of new treatments.
Highlights
The metabolic alterations of cancer cells, that distinguish them from healthy cells, are recognized as one of the ten hallmarks of cancer
As this review focuses on the disturbed glucose metabolism, we refer the interested reader to our recently published review that describes the role of glutamine in lung cancer [7]
Due to the metabolic plasticity exhibited by cancer cells, it is not unexpected that tumor cells could develop resistance to inhibition of a specific pathway through upregulation of alternative pathways
Summary
The metabolic alterations of cancer cells, that distinguish them from healthy cells, are recognized as one of the ten hallmarks of cancer. Lung cancer cells are characterized by expression of a dimeric form of PKM2 which implies that all glycolytic intermediates preceding PKM2 activity accumulate and are directed into biosynthetic processes, such as nucleotide-, lipidand serine/glycine synthesis which stimulates tumor proliferation as demonstrated in Figure 1 [27,28,29].
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