Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8429264 | Biochimica et Biophysica Acta (BBA) - Reviews on Cancer | 2018 | 28 Pages |
Abstract
Altered cellular metabolism is a hallmark of cancer. Cancer cells express isoforms of metabolic enzymes that may constitute therapeutic targets. Glutaminase controls glutamine metabolism and their expression correlate with malignancy of tumours. The two types of glutaminase isoenzymes, GLS and GLS2, differ in their expression patterns and functional roles: GLS has oncogenic properties and GLS2 has been described as a tumour suppressor factor. Selective genomic and epigenomic intervention over glutaminase affects the metabolic reprogramming of cancer. This review highlights the molecular metabolic vulnerabilities in various types of cancer, to be used for biomarker development, drug design, and in personalized oncology.
Keywords
GlcPKBGLNLGAGLSGABKGAGDHERKRT-qPCROXPHOSGSHPKM2Combinatory therapyEATCNF-κBPI3Kpyruvate kinase M2 isoformEhrlich ascites tumour cellsPDAGACIDH12HGPFKFB32-HydroxyglutarateROSStat1Pancreatic ductal adenocarcinomamalic enzymeMetabolic reprogrammingDONCancer metabolismNuclear factor-kappa Bphosphatidylinositide 3-kinaseOxidative phosphorylationsignal transducer and activator of transcription 1real-time quantitative polymerase chain reactionprotein kinase Bpyruvate carboxylaseextracellular signal-regulated kinasesGluGlutathioneglutamateglutamate dehydrogenaseglutamineGlutamine synthetaseGlutaminaseGlucoseReactive oxygen species
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Authors
José M. Matés, José A. Campos-Sandoval, Javier Márquez,