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Curr Opin Genet Dev. 2016 Jun;38:102-109. doi: 10.1016/j.gde.2016.05.003. Epub 2016 Jun 5.

Mitochondrial pyruvate carrier function and cancer metabolism.

Author information

1
Department of Biochemistry, Fraternal Order of the Eagles Diabetes Research Center, Abboud Cardiovascular Research Center, Holden Comprehensive Cancer Center, and Pappajohn Biomedical Institute, University of Iowa Carver College of Medicine, Iowa City, IA 52242, USA.
2
Department of Biochemistry, Fraternal Order of the Eagles Diabetes Research Center, Abboud Cardiovascular Research Center, Holden Comprehensive Cancer Center, and Pappajohn Biomedical Institute, University of Iowa Carver College of Medicine, Iowa City, IA 52242, USA. Electronic address: eric-taylor@uiowa.edu.

Abstract

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.

PMID:
27269731
PMCID:
PMC5017534
DOI:
10.1016/j.gde.2016.05.003
[Indexed for MEDLINE]
Free PMC Article

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