Egr-1 Promotes Cell Proliferation and Invasion by Increasing β-Catenin Expression in Gastric Cancer

Abnormal expression of early growth response gene 1 (Egr-1) and beta-catenin may play a crucial role in the development and progression of human cancer. However, little is known about the expression and underlying molecular mechanisms in which Egr-1 and beta-catenin are involved in the development and progression of gastric cancer. The purpose of this study was to elucidate the potential relationship between Egr-1 and beta-catenin expression in gastric cancer, which contributes to finding new molecular carcinogenesis as a potential therapeutic target for gastric cancer. In a sample of 102 cases of human gastric cancer, the expression of Egr-1 and beta-catenin was detected using immunohistochemistry. Egr-1 gene was transfected into gastric cancer SGC7901 cells and its role in proliferation and cell invasion was detected by MTT assay, flow cytometry, wound-healing and transwell invasion assay. Western blot analysis was used to study the expression of beta-catenin and cyclin D1 proteins. Upregulated Egr-1 and beta-catenin protein expression were strongly correlated with cancer progression and depth of invasion in gastric cancer. beta-catenin, present mainly in cytoplasmic and nucleus of gastric cancer cells, was also positively correlated with Egr-1 expression in gastric cancer. Furthermore, the overexpression of Egr-1 upregulated beta-catenin expression level, promoted cell proliferation, increased cell population in S-phase and enhanced gastric cancer cell migration and invasion in vitro. Egr-1 might contribute to gastric cancer proliferation and invasion through activation of the beta-catenin signaling pathway.