Mitochondrial pyruvate carrier function and cancer metabolism

被引:45
作者
Rauckhorst, Adam J.
Taylor, Eric B. [1 ]
机构
[1] Univ Iowa, Abboud Cardiovasc Res Ctr, Fraternal Order Eagles Diabet Res Ctr, Dept Biochem,Holden Comprehens Canc Ctr,Carver Co, Iowa City, IA 52242 USA
关键词
LUNG-CANCER; LACTATE-DEHYDROGENASE; GLUTAMINE-METABOLISM; AEROBIC GLYCOLYSIS; GLUCOSE-METABOLISM; HUMAN GLIOBLASTOMA; TUMOR-CELLS; GROWTH; TRANSPORT; DICHLOROACETATE;
D O I
10.1016/j.gde.2016.05.003
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Metabolic reprogramming in cancer supports the increased biosynthesis required for unchecked proliferation. Increased glucose utilization is a defining feature of many cancers that is accompanied by altered pyruvate partitioning and mitochondrial metabolism. Cancer cells also require mitochondrial tricarboxylic acid cycle activity and electron transport chain function for biosynthetic competency and proliferation. Recent evidence demonstrates that mitochondrial pyruvate carrier (MPC) function is abnormal in some cancers and that increasing MPC activity may decrease cancer proliferation. Here we examine recent findings on MPC function and cancer metabolism. Special emphasis is placed on the compartmentalization of pyruvate metabolism and the alternative routes of metabolism that maintain the cellular biosynthetic pools required for unrestrained proliferation in cancer.
引用
收藏
页码:102 / 109
页数:8
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