Current Journal of Applied Science and Technology

Zinc is an essential trace element whose influence on human physiology extends from the structural scaffolding of proteins to the catalytic chemistry of enzymes that govern DNA replication and repair, transcriptional regulation, antioxidant defence, and immune signalling. A growing body of epidemiological, clinical, and mechanistic evidence suggests that zinc deficiency, which affects roughly one-fifth of the world's population, contributes meaningfully to cancer initiation and progression through several interlocking molecular routes. Disrupted zinc homeostasis weakens p53 tumour suppressor function, drives oxidative DNA damage, impairs apoptotic signalling, and alters the expression of zinc transporters in ways that switch on oncogenic kinase cascades. Reduced zinc availability also leaves an epigenetic footprint, changing histone deacetylase activity and compromising the integrity of zinc finger proteins. At the same time, the very enzymes that become overexpressed or functionally deranged in malignant cells — matrix metalloproteinases, carbonic anhydrases, and histone deacetylases among them — depend on zinc for catalysis and structural stability, which makes the zinc-coordination site within these proteins an attractive point of pharmacological attack. Molecular docking, a computational approach for predicting how small molecules bind within protein active sites, has become a practical and relatively inexpensive tool for discovering and refining inhibitors of these zinc-dependent cancer targets. This review brings together current understanding of how zinc deficiency promotes cancer progression at the molecular level, examines the structural features of the principal zinc-dependent oncological targets, and assesses what molecular docking has, and has not, achieved in the rational design of inhibitors for these proteins. The technical difficulties of modelling zinc–ligand coordination computationally are considered alongside emerging solutions, and the review closes by identifying gaps in the literature and opportunities for work that connects nutritional biochemistry, cancer cell biology, and computer-aided drug design.