Abstract
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.
Highlights
Gastric cancer (GC) is a malignant tumor that originates from the epithelium of the gastric mucosa
In order to clarify the mechanism of Metallothionein 1G (MT1G) in GC, we analyzed its expression in tissues of GC
MT1G is a DNA methylation-related gene which is reported to play an important role in various types of cancer (Henrique et al, 2005; Roth et al, 2006; Sakamoto et al, 2010; Arriaga et al, 2012; Fu et al, 2013; Zeng et al, 2018)
Summary
Gastric cancer (GC) is a malignant tumor that originates from the epithelium of the gastric mucosa. It ranks first among various malignant tumors in China. The only treatment for gastric cancer is surgical resection (Kai et al, 2018). The early symptoms of gastric cancer are difficult to detect, so majority of patients with gastric cancer are difficult to diagnose early, and losing the chance of cure and resection. Even chemotherapy is used as a clinical treatment method for gastric cancer, but GC has a strong ability to metastasize, so the prognosis of GC patients is still very poor (Peng et al, 2018). Studying the mechanism and process of GC can be better used for clinical treatment and diagnosis of GC (Waldum and Fossmark, 2018)
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