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Mitochondrial pyruvate carrier function and cancer metabolism
Journal article   Peer reviewed

Mitochondrial pyruvate carrier function and cancer metabolism

Adam J Rauckhorst and Eric B Taylor
Current opinion in genetics & development, Vol.38, pp.102-109
06/2016
DOI: 10.1016/j.gde.2016.05.003
PMCID: PMC5017534
PMID: 27269731

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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.
Neoplasms - metabolism Mitochondrial Membrane Transport Proteins Cell Proliferation - genetics Citric Acid Cycle - genetics Monocarboxylic Acid Transporters Mitochondria - genetics Neoplasms - genetics Membrane Transport Proteins - genetics Electron Transport - genetics Humans Pyruvic Acid - metabolism Mitochondria - metabolism

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