Metabolic adaptation to cancer growth: from the cell to the organism.

Xavier Escoté, Lluís Fajas

Journal: Cancer letters 2015;356(2 Pt A):171-5

PMID: 24709629

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Abstract

Tumour cells proliferate much faster than normal cells; nearly all anticancer treatments are toxic to both cell types, limiting their efficacy. The altered metabolism resulting from cellular transformation and cancer progression supports cellular proliferation and survival, but leaves cancer cells dependent on a continuous supply of energy and nutrients. Hence, many metabolic enzymes have become targets for new cancer therapies. In addition to its well-described roles in cell-cycle progression and cancer, the cyclin/CDK-pRB-E2F1 pathway contributes to lipid synthesis, glucose production, insulin secretion, and glycolytic metabolism, with strong effects on overall metabolism. Notably, these cell-cycle regulators trigger the adaptive "metabolic switch" that underlies proliferation.

Address: Department of Physiology, Université de Lausanne, Lausanne, Switzerland. Electronic address: [email protected].; Department of Physiology, Université de Lausanne, Lausanne, Switzerland. Electronic address: [email protected].

DOI: 10.1016/j.canlet.2014.03.034

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MeSH Terms: Cell Cycle Checkpoints, Cell Proliferation, Cyclin-Dependent Kinases, Cyclins, E2F1 Transcription Factor, Energy Metabolism, Fatty Acids, Glycolysis, Humans, Lipids, Neoplasms, Retinoblastoma Protein