Metabolic adaptation to cancer growth: from the cell to the organism.
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.
Department of Physiology, Université de Lausanne, Lausanne, Switzerland. Electronic address: xavier.escote@unil.ch.
Xavier
X
Escoté
Department of Physiology, Université de Lausanne, Lausanne, Switzerland. Electronic address: lluis.fajas@unil.ch.
Lluís
L
Fajas
D059447:Cell Cycle Checkpoints; D049109:Cell Proliferation; D018844:Cyclin-Dependent Kinases / Q000378:metabolism*; D016213:Cyclins / Q000378:metabolism; D050687:E2F1 Transcription Factor / Q000378:metabolism*; D004734:Energy Metabolism / Q000502:physiology*; D005227:Fatty Acids / Q000378:metabolism; D006019:Glycolysis / Q000502:physiology; D006801:Humans; D008055:Lipids / Q000096:biosynthesis; D009369:Neoplasms / Q000378:metabolism* / Q000473:pathology*; D016160:Retinoblastoma Protein / Q000378:metabolism
D016213:Cyclins; D050687:E2F1 Transcription Factor; C493753:E2F1 protein, human; D005227:Fatty Acids; D008055:Lipids; D016160:Retinoblastoma Protein; D018844:Cyclin-Dependent Kinases
Cdk4; Cell cycle; E2F1 transcription factor; Glucose; Glycolysis; Metabolism