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Metallothionein (  MT1M  ) belongs to a family of cysteine-rich cytosolic protein and has been reported to be a tumor suppressor gene in multiple cancers. However, its role in esophageal carcinoma carcinogenesis remains unclear. In this study,  MT1M  expression was correlated with tumor type, stage, drinking and smoking history, as well as patient survival. We also studied the regulation and biological function of  MT1M  in esophageal squamous cell carcinoma (ESCC). We have found that  MT1M  is significantly downregulated in ESCC tissues compared with adjacent non-cancer tissues. Furthermore, restoration of expression by treatment with the demethylation agent A + T showed that  MT1M  downregulation might be closely related to hypermethylation in its promoter region. Over-expression of  MT1M  in ESCC cells significantly altered cell morphology, induced apoptosis, and reduced colony formation, cell viability, migration and epithelial-mesenchymal transition. Moreover, based on reactive oxygen species (  ROS  ) levels, a superoxide dismutase 1 (  SOD1  ) activity assay and protein analysis, we verified that the tumor-suppressive function of  MT1M  was at least partially caused by its upregulation of  ROS  levels, downregulation of  SOD1  activity and phosphorylation of the  SOD1  downstream pathway  PI3K/AKT  . In conclusion, our results demonstrated that  MT1M  was a novel tumor-suppressor in ESCC and may be disrupted by promoter CpG methylation during esophageal carcinogenesis.

molecules and cells/molecules and cells

Metallothionein <i>MT1M</i> Suppresses Carcinogenesis of Esophageal Carcinoma Cells through Inhibition of the Epithelial-Mesenchymal Transition and the <i>SOD1/PI3K</i> Axis

Metallothionein MT1M Suppresses Carcinogenesis of Esophageal Carcinoma Cells through Inhibition of the Epithelial-Mesenchymal Transition and the SOD1/PI3K Axis