Targeting cellular metabolism to improve cancer therapeutics

The metabolic properties of cancer cells diverge significantly from those of normal cells. Energy production in cancer cells is abnormally dependent on aerobic glycolysis. In addition to the dependency on glycolysis, cancer cells have other atypical metabolic characteristics such as increased fatty...

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Bibliographic Details
Published in:Cell death & disease 2013-03, Vol.4 (3), p.e532-e532
Main Authors: Zhao, Y, Butler, E B, Tan, M
Format: Article
Language:English
Subjects:
631/80/82/23
692/699/67/1059/2326
692/699/67/1059/602
692/699/67/2327
Antibodies
Biochemistry
Biomedical and Life Sciences
Cell Biology
Cell Culture
Drug Resistance, Neoplasm
Fatty Acid Synthases - antagonists & inhibitors
Fatty Acid Synthases - metabolism
Glucose Transport Proteins, Facilitative - antagonists & inhibitors
Glucose Transport Proteins, Facilitative - metabolism
Glutaminase - antagonists & inhibitors
Glutaminase - metabolism
Hexokinase - antagonists & inhibitors
Hexokinase - metabolism
Humans
Immunology
Isoenzymes - antagonists & inhibitors
Isoenzymes - metabolism
L-Lactate Dehydrogenase - antagonists & inhibitors
L-Lactate Dehydrogenase - metabolism
Life Sciences
Neoplasms - metabolism
Neoplasms - pathology
Neoplasms - therapy
Protein-Serine-Threonine Kinases - antagonists & inhibitors
Protein-Serine-Threonine Kinases - metabolism
Pyruvate Kinase - antagonists & inhibitors
Pyruvate Kinase - metabolism
Review
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Description
Summary:The metabolic properties of cancer cells diverge significantly from those of normal cells. Energy production in cancer cells is abnormally dependent on aerobic glycolysis. In addition to the dependency on glycolysis, cancer cells have other atypical metabolic characteristics such as increased fatty acid synthesis and increased rates of glutamine metabolism. Emerging evidence shows that many features characteristic to cancer cells, such as dysregulated Warburg-like glucose metabolism, fatty acid synthesis and glutaminolysis are linked to therapeutic resistance in cancer treatment. Therefore, targeting cellular metabolism may improve the response to cancer therapeutics and the combination of chemotherapeutic drugs with cellular metabolism inhibitors may represent a promising strategy to overcome drug resistance in cancer therapy. Recently, several review articles have summarized the anticancer targets in the metabolic pathways and metabolic inhibitor-induced cell death pathways, however, the dysregulated metabolism in therapeutic resistance, which is a highly clinical relevant area in cancer metabolism research, has not been specifically addressed. From this unique angle, this review article will discuss the relationship between dysregulated cellular metabolism and cancer drug resistance and how targeting of metabolic enzymes, such as glucose transporters, hexokinase, pyruvate kinase M2, lactate dehydrogenase A, pyruvate dehydrogenase kinase, fatty acid synthase and glutaminase can enhance the efficacy of common therapeutic agents or overcome resistance to chemotherapy or radiotherapy.
ISSN:2041-4889
2041-4889
DOI:10.1038/cddis.2013.60