Abstract
OBJECTIVE: The aim of the study is to determine the role of nuclear receptor coactivator 2 in cell proliferation and invasion ability of gastric cancer cells and to explore its possible mechanisms. METHODS: Immunohistochemical staining was used to determine NCOA2 gene expression in gastric cancer. Western blotting was used to detect Wnt signal pathways-related protein expression. Colony formation assays, Cell Counting Kit-8 assays, and transwell assays were used to determine cell proliferation, metastasis, and invasion ability of gastric cancer cells. A flow cytometric apoptosis tests determine gastric cancer cell apoptosis ability after inhibition of the expression of nuclear receptor coactivator 2. Subcutaneous mouse models were used to determine the gastric cancer growth and peritoneal metastasis differences after inhibition the expression of nuclear receptor coactivator 2. RESULTS: The expression of nuclear receptor coactivator 2 in gastric cancer cells is high (P < .01), including lymph node metastasis, TNM staging, and gender differences in nuclear receptor coactivator 2 expression were statistically significant (P < .01). Short interfering nuclear receptor coactivator 2 could inhibit the proliferation and invasion ability of gastric cancer cells. Short interfering nuclear receptor coactivator 2 promotes the apoptosis of gastric cancer cells. Animal experiments showed that short interfering nuclear receptor coactivator 2 could inhibit the growth and invasion of gastric cancer-transplantable tumors. Knockdown of the expression of nuclear receptor coactivator 2 inhibited the Wnt/β-catenin signaling pathway in the gastric cancer cells. CONCLUSIONS: Knockdown of the expression of nuclear receptor coactivator 2 can inhibit the proliferation and invasion of human gastric cancer in vitro and in vivo. The underlying mechanism of NOCA2 affects the Wnt signaling pathway.