Cadmium (Cd) contamination in agricultural soils severely threatens crop productivity and food safety. Mung bean (Vigna radiata), a globally important legume, is highly susceptible to Cd toxicity, which disrupts nutrient homeostasis, photosynthesis, and redox balance. Melatonin (Mel), a pleiotropic signaling molecule, has emerged as a potential mitigator of abiotic stresses, but its mechanisms of Cd tolerance in mung bean remain poorly understood. Here, we demonstrate that Mel alleviates Cd toxicity by: (1) facilitating internal Cd sequestration by promoting its deposition in the leaf cell wall and vacuolar compartmentalization, a process mediated by the upregulation of key transporter genes PCR2 (Plant Cadmium Resistance 2) and HMA (Heavy Metal ATPase); (2) restricting Cd entry into the plant by downregulating the expression of root metal influx transporters, namely ZIP1 (Zinc-regulated, Iron-regulated Transporter-like Protein 1) and YSL3 (Yellow Stripe-Like 3); and (3) counteracting Cd-induced nutritional deficits achieved through the activation of plasma membrane H+-ATPase and the enhancement of the nitrate reductase (NR)/glutamine synthetase-glutamate synthase (GS-GOGAT) pathway. Concurrently, Mel treatment robustly improved redox homeostasis by significantly boosting the activities of major antioxidant enzymes (SOD; CAT; APX) and stimulating the biosynthesis of phytochelatins for Cd chelation. Genome-wide transcriptomic profiling further corroborated these physiological observations, revealing Mel's targeted regulation of a comprehensive gene network implicated in metal trafficking, cell wall fortification, and reactive oxygen species (ROS) scavenging. Overall, this work provides novel insights into the mechanistic basis of Mel-induced Cd tolerance and underscores its potential as an effective agro-biotechnological strategy for safeguarding crop plants in metal-contaminated environments.