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The glutamate/cystine xCT antiporter antagonizes glutamine metabolism and reduces nutrient flexibility
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The glutamate/cystine xCT antiporter antagonizes glutamine metabolism and reduces nutrient flexibility
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Journal Article
The glutamate/cystine xCT antiporter antagonizes glutamine metabolism and reduces nutrient flexibility
2017
Overview
As noted by Warburg, many cancer cells depend on the consumption of glucose. We performed a genetic screen to identify factors responsible for glucose addiction and recovered the two subunits of the xCT antiporter (system x
c
−
), which plays an antioxidant role by exporting glutamate for cystine. Disruption of the xCT antiporter greatly improves cell viability after glucose withdrawal, because conservation of glutamate enables cells to maintain mitochondrial respiration. In some breast cancer cells, xCT antiporter expression is upregulated through the antioxidant transcription factor Nrf2 and contributes to their requirement for glucose as a carbon source. In cells carrying patient-derived mitochondrial DNA mutations, the xCT antiporter is upregulated and its inhibition improves mitochondrial function and cell viability. Therefore, although upregulation of the xCT antiporter promotes antioxidant defence, it antagonizes glutamine metabolism and restricts nutrient flexibility. In cells with mitochondrial dysfunction, the potential utility of xCT antiporter inhibition should be further tested.
The factors that limit the nutrient flexibility of cells remain largely unknown. Here, the authors identify the glutamate/cysteine antiporter xCT in a genetic screen for glucose dependency and show it determines the ability of cells to survive under conditions of low glucose by limiting the utilization of glutamine.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/106
/ 38
/ 82
/ 82/80
/ Amino Acid Transport System y+ - genetics
/ Amino Acid Transport System y+ - metabolism
/ Carbon
/ Cloning
/ Culture Media - pharmacology
/ Epithelial Cells - drug effects
/ Epithelial Cells - metabolism
/ Epithelial Cells - pathology
/ Gene Expression Regulation, Neoplastic
/ Glucose
/ Humanities and Social Sciences
/ Humans
/ Kinases
/ Mutation
/ NF-E2-Related Factor 2 - genetics
/ NF-E2-Related Factor 2 - metabolism
/ Oxidative Phosphorylation - drug effects
/ Science
