MT1A

Metallothionein 1A (MT1A), also known as MT-1A or MT1, is a cysteine-rich, low-molecular-weight protein critical for metal ion homeostasis and detoxification. It binds heavy metals such as zinc, cadmium, and copper via thiolate clusters, modulating cellular redox balance and mitigating oxidative stress. MT1A participates in metal trafficking, apoptosis regulation, and inflammatory responses. Its activity intersects with pathways including the Nrf2-Keap1 antioxidant response, NF-κB signaling, and p53-mediated stress responses. Dysregulation of MT1A has been implicated in hepatocellular carcinoma, neurodegenerative disorders (e.g., Alzheimer’s), and cadmium-induced nephrotoxicity due to altered metal buffering or impaired ROS scavenging.
Elevated MT1A expression is observed in drug-resistant cancers, where it may counteract platinum-based chemotherapy by sequestering cytotoxic metal ions. Conversely, MT1A deficiency exacerbates metal toxicity and oxidative tissue damage. Therapeutic strategies targeting MT1A include small-molecule modulators to enhance chemosensitivity or mitigate neurotoxicity in metal-overload conditions. Recent studies explore MT1A as a biomarker for early cancer detection and a potential target for metallodrug delivery systems. However, its dual role in cytoprotection and pathological metal retention complicates drug development, necessitating context-specific therapeutic approaches.