Abstract
Reprogramming of cell metabolism is essential for tumorigenesis, and is regulated by a complex network, in which PKM2 plays a critical role. PKM2 exists as an inactive monomer, less active dimer and active tetramer. While dimeric PKM2 diverts glucose metabolism towards anabolism through aerobic glycolysis, tetrameric PKM2 promotes the flux of glucose-derived carbons for ATP production via oxidative phosphorylation. Equilibrium of the PKM2 dimers and tetramers is critical for tumorigenesis, and is controlled by multiple factors. The PKM2 dimer also promotes aerobic glycolysis by modulating transcriptional regulation. We will discuss the current understanding of PKM2 in regulating cancer metabolism.
Keywords:
Aerobic glycolysis; Cancer metabolism; Cell signalling; PKM2.
Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Carrier Proteins / biosynthesis
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Carrier Proteins / genetics
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Carrier Proteins / metabolism*
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Cell Proliferation
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Cell Transformation, Neoplastic / pathology
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Gene Expression Regulation, Neoplastic
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Glucose / metabolism
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Glycolysis / physiology*
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Humans
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Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
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Membrane Proteins / biosynthesis
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Membrane Proteins / genetics
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Membrane Proteins / metabolism*
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Neoplasm Proteins / biosynthesis
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Neoplasm Proteins / genetics
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Neoplasm Proteins / metabolism*
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Neoplasms / metabolism*
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Neoplasms / pathology
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Proto-Oncogene Proteins c-myc / metabolism
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Thyroid Hormone-Binding Proteins
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Thyroid Hormones / biosynthesis
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Thyroid Hormones / genetics
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Thyroid Hormones / metabolism*
Substances
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Carrier Proteins
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HIF1A protein, human
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Hypoxia-Inducible Factor 1, alpha Subunit
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MYC protein, human
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Membrane Proteins
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Neoplasm Proteins
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Proto-Oncogene Proteins c-myc
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Thyroid Hormones
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Glucose