TY - JOUR
T1 - Metabolic changes associated with tumor metastasis, part 2 - Mitochondria, lipid and amino acid metabolism
AU - Porporato, Paolo E.
AU - Payen, Valery L.
AU - Baselet, Bjorn
AU - Sonveaux, Pierre
N1 - Score=10
PY - 2015/11/23
Y1 - 2015/11/23
N2 - Metabolic alterations are a hallmark of cancer controlling tumor progression and metastasis. Among the various metabolic phenotypes encountered in tumors, this review focuses on the contributions of mitochondria, lipid and amino acid metabolism to the metastatic process. Tumor cells require functional mitochondria to grow, proliferate and metastasize, but shifts in mitochondrial activities confer pro-metastatic traits encompassing increased production of mitochondrial reactive oxygen species (mtROS), enhanced resistance to apoptosis and the increased or de novo production of metabolic intermediates of the TCA cycle behaving as oncometabolites, including succinate, fumarate, and D-2-hydroxyglutarate that control energy production, biosynthesis and the redox state. Lipid metabolism and the metabolism of amino acids, such as glutamine, glutamate and proline are also currently emerging as focal control points of cancer metastasis.
AB - Metabolic alterations are a hallmark of cancer controlling tumor progression and metastasis. Among the various metabolic phenotypes encountered in tumors, this review focuses on the contributions of mitochondria, lipid and amino acid metabolism to the metastatic process. Tumor cells require functional mitochondria to grow, proliferate and metastasize, but shifts in mitochondrial activities confer pro-metastatic traits encompassing increased production of mitochondrial reactive oxygen species (mtROS), enhanced resistance to apoptosis and the increased or de novo production of metabolic intermediates of the TCA cycle behaving as oncometabolites, including succinate, fumarate, and D-2-hydroxyglutarate that control energy production, biosynthesis and the redox state. Lipid metabolism and the metabolism of amino acids, such as glutamine, glutamate and proline are also currently emerging as focal control points of cancer metastasis.
KW - Electron transport chain (ETC)
KW - Glutaminolysis
KW - Lipogenesis
KW - Oxidative phosphorylation (OXPHOS)
KW - Proline metabolism
KW - Reactive oxygen species (ROS)
KW - Tricarboxylic acid cycle (TCA cycle)
KW - Tumor metastasis
UR - http://ecm.sckcen.be/OTCS/llisapi.dll/open/20018335
UR - https://www.ncbi.nlm.nih.gov/pubmed/26646069
U2 - 10.1007/s00018-015-2100-2
DO - 10.1007/s00018-015-2100-2
M3 - Article
SN - 1420-682X
VL - 73
JO - Cellular and Molecular Life Science
JF - Cellular and Molecular Life Science
IS - 7
ER -