MT1G inhibits the growth and epithelial-mesenchymal transition of gastric cancer cells by regulating the PI3K/AKT signaling pathway



Título del documento: MT1G inhibits the growth and epithelial-mesenchymal transition of gastric cancer cells by regulating the PI3K/AKT signaling pathway
Revue: Genetics and molecular biology
Base de datos: PERIÓDICA
Número de sistema: 000459233
ISSN: 1415-4757
Autores: 1
2
2
1
Instituciones: 1First Affiliated Hospital of Gannan Medical University, Department of Gastroenterology, Ganzhou, Jiangxi. China
2First Affiliated Hospital of Gannan Medical University, Department of Gastrointestinal Surgery, Ganzhou, Jiangxi. China
Año:
Volumen: 45
Número: 1
País: Brasil
Idioma: Inglés
Tipo de documento: Artículo
Enfoque: Experimental, analítico
Resumen en inglés Gastric carcinoma (GC) is a malignant tumor that has high mortality and morbidity worldwide. Although many efforts have been focused on the development and progression of GC, the underlying functional regulatory mechanism of GC needs more clarification. Metallothionein 1G (MT1G) is a member of the metallothionein family (MTs), and hypermethylation of MT1G occurred in a variety of cancers, including gastric cancer. However, the functional mechanism of MT1G in GC remains unclear. Here, we demonstrated that MT1G was down-regulated in GC tissues and cells. Overexpression of MT1G inhibited cell proliferation, foci formation and cell invasion, while knockdown of MT1G increased cell proliferation, foci formation and cell invasion. In addition, MT1G overexpression inhibited cell cycle progression and MT1G deficiency exerted opposite phenotype. p-AKT was negatively regulated by MT1G. In summary, our study reveals that MT1G exerts crucial role in regulating of cell proliferation and migration of gastric cancer, providing new insights for MT1G-related pathogenesis and a basis for developing new strategies for treatment of GC
Disciplinas: Biología,
Medicina
Palabras clave: Genética,
Oncología,
PI3K/AKT,
GC,
MT1G,
Cáncer gástrico
Keyword: Genetics,
Oncology,
MT1G,
GC,
PI3K/AKT,
Gastric cancer
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