MT1B overexpression enhances malignancy of A549 non-small cell lung cancer cells.

Metallothioneins (MTs) are metal-binding proteins that are involved in heavy metal homeostasis and protection against oxidative stress. The MT1 family comprises several isoforms that are implicated in various diseases, including cancer. Although the dysregulated expression of MT1 isoforms has been observed in lung cancer, the specific role of MT isoform MT1B remains unclear. To investigate the role of MT1B in lung cancer progression, A549 lung cancer cells were transfected with an MT1B expression vector. In vitro assays were performed to assess cell viability, migration, invasion, and colony formation. Western blot analysis revealed increased expression of epithelial-mesenchymal transition (EMT) markers Snail, Vimentin, and N-cadherin, and decreased levels of E-cadherin, indicating EMT induction. In the xenograft model, the MT1Btransfected group formed tumors more rapidly and exhibited significantly increased tumor growth compared to the controls. In addition, RNA sequencing was performed to identify MT1Bdependent gene alterations, and Ingenuity Pathway Analysis (IPA) was applied to characterize the canonical pathways and predicted biological functions associated with these MT1Bspecific genes. These findings suggest that cellular MT1B overexpression has the potential to promote lung cancer growth. [BMB Reports 2026; 59(2): 161-168].