NIT2 (nitrilase family member 2) is a cytosolic omega-amidase enzyme with dual functions in metabolism and tumor suppression. Primary metabolic function: NIT2 catalyzes hydrolysis of α-ketoglutaramate and α-ketosuccinamate to produce α-ketoglutarate and oxaloacetate, respectively, thereby linking sulfur metabolism to the tricarboxylic acid cycle 1. The enzyme contains a catalytic triad (E43, K112, C153) essential for substrate binding and catalytic activity 1. Mechanism: NIT2 activity is redox-sensitive, with reversible oxidation of cysteine residues impairing catalytic function under oxidative stress 2. Beyond metabolism, NIT2 exhibits tumor-suppressive properties through non-metabolic mechanisms: it inhibits cell growth via G2 arrest by upregulating 14-3-3sigma 3 and restrains oxidative phosphorylation by inhibiting BRD1-mediated histone acetylation 4. Disease relevance: NIT2 expression inversely correlates with chemoresistance in gastric cancer, where depletion promotes 5-FU resistance 4. Paradoxically, NIT2 overexpression predicts poor prognosis in tongue squamous cell carcinoma 5, and genetic variants increasing NIT2 expression elevate lung adenocarcinoma risk 6. Clinical significance: NIT2 loss impairs endothelial angiogenesis and induces senescence 2, suggesting therapeutic potential in cancer chemosensitization and vascular dysfunction.