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Its proposed mechanisms involve multiple cytoprotective pathways including upregulation of VEGF and growth factors promoting angiogenesis, modulation of the nitric oxide system, activation of the FAK-paxillin pathway for cell migration and tissue repair, interaction with the gut-brain axis affecting dopaminergic and serotonergic systems, and gastroprotective effects against NSAID and alcohol-induced mucosal damage

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To investigate whether S-nitrosylation of MYCN at specific cysteine residues contributes to NO-mediated suppression of ER stress in NEPC, we generated site-directed mutations at Cys4, Cys186, and Cys464 (Supplementary Fig

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