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Noch Lab

GBM cells exhibit a unique susceptibility to cysteine. I have shown that cysteine induces mitochondrial reductive stress in GBM through H2O2 production. Through TCGA and CPTAC analyses, I found that GBM exhibits high cysteine gene expression and low mitochondrial redox enzyme expression, likely underlying this susceptibility (Fig. 2). Understanding the mechanism of redox enzyme downregulation in GBM and the functional significance that altered redox enzyme expression has on cysteine susceptibility is critical to effective targeting of this pathway. I will test the hypotheses that redox enzyme deficiency underlies cysteine susceptibility in GBM by 1) by inducing global changes in reactive cysteine residues in metabolic enzymes and 2) by altering glycolytic and mitochondrial TCA flux (Fig. 1).

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