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논문 기본 정보

자료유형
학술저널
저자정보
Lin Ye (The First Affiliated Hospital of Chongqing Medical University) Dandan Li (The First Affiliated Hospital of Chongqing Medical University) Weiyan Peng (The First Affiliated Hospital of Chongqing Medical University) Bin Wu (The First Affiliated Hospital of Chongqing Medical University) Huan Liu (The First Affiliated Hospital of Chongqing Medical University) Ruizhen Zhang (Daping Hospital Army Medical University) Ruiqin Zhou (The First Affiliated Hospital of Chongqing Medical University) Lijun Yao (The First Affiliated Hospital of Chongqing Medical University)
저널정보
한국분자세포생물학회 Molecules and Cells Molecules and Cells 제44권 제4호
발행연도
2021.1
수록면
267 - 278 (12page)

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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.

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