Back to article: MYCN upregulates the transsulfuration pathway to suppress the ferroptotic vulnerability in MYCN-amplified neuroblastoma
FIGURE 3: Suggested model for the metabolic pathways that lead to accumulation of cysteine and ultimately to glutathione (GSH) and inhibition of lipid peroxidation in MYCN-amplified neuroblastomas. Cysteine can derive either (1) from cystine that is imported by system xc-, or (2) from cystathionine that is produced from methionine through the transsulfuration pathway. To provide adequate fuel molecules to the transsulfuration pathway, MYCN orchestrates the induction of the key enzymes CBS and MTAP.