[Energy metabolism of the cancer cell: example of mitochondria-rich endocrine tumors].
Most solid tumours preferentially develop glycolytic metabolism, often accompanying tumor aggressiveness. Increase in nucleic acid synthesis is associated with cell proliferation and glucose shunting to the pentose phosphate pathway. High glucose consumption is more associated with a metabolic adaptation than with a mitochondrial defect. Tumor cells do not present specific genetic modifications but adapt their metabolic capacities to their priority needs. However their metabolisms depend on oncogene expression more specifically expressed in this context. The glycolytic pathway is favored by tumor proliferation under hypoxia. Stabilization of HIF1 factor may explain the glycolytic metabolism of the tumors in an anaerobic environment. We demonstrate in two types of mitochondrial rich tumors, that specific defects induce completely different metabolic directions: when familial paragangliomas present a glycolytic metabolism, thyroid oncocytic tumors develop a specific oxidative metabolism.
Malthièry
Y
Y
Inserm U 694, Biochimie et Biologie moléculaire, CHU, 4, rue Larrey, 49033 Angers Cedex. Yvmalthiery@chu-angers.fr
Savagner
F
F
D004701:Endocrine Gland Neoplasms / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology / Q000648:ultrastructure; D004734:Energy Metabolism / Q000502:physiology*; D005943:Gluconeogenesis / Q000502:physiology; D005947:Glucose / Q000378:metabolism; D006019:Glycolysis / Q000502:physiology; D006801:Humans; D008928:Mitochondria / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology; D010427:Pentose Phosphate Pathway
D005947:Glucose