ARHGAP9 siRNA inhibits gastric cancer cell proliferation and EMT via inactivating Akt, p38 signaling and inhibiting MMP2 and MMP9

被引：2
作者：
Sun, Lingjia [1 ]
Zhang, Youping [1 ]
Lou, Jie [1 ]
机构：
[1] Ningbo 2 Hosp, Dept Gastroenterol, 41 Xibei Rd, Ningbo 315010, Zhejiang, Peoples R China
来源：
INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY | 2017年 / 10卷 / 12期
关键词：
ARHGAP9; epithelial to mesenchymal transition; E-cadherin; SGC7901; EPITHELIAL-MESENCHYMAL TRANSITION; E-CADHERIN; RHO-GTPASE; INVASION; PATHWAY; GENE;
D O I：
暂无
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Objective: ARHGAP9 is a RhoGTPase activating protein. This study aimed to investigate the effect of ARHGAP9 on cell proliferation of gastric cancer cell. Methods: Human gastric cancer cell line SGC7901 were transfected with ARHGAP9 siRNA and the expression of epithelial to mesenchymal transition (EMT) factors, MMPs, and activated status of Akt and p38 signaling were detected. Moreover, the migration, invasion, and viability of SGC7901 cells were determined. Results: ARHGAP9 siRNA successfully inhibited cell viability, migration and invasion. The expression of E-cadherin was significantly upregulated, and expression of Snail, Vimentin, as well as MMP2 and MMP9 were obviously downregulated. Moreover, ARHGAP9 siRNA promoted inactivation of Akt and p38 signaling by inhibiting expression of p-Akt and p-p38. Conclusion: This study showed that ARHGAP9 contributed to the viability, migration, invasion as well as EMT in gastric cancer cell line SGC7901. ARHGAP9 might be used as a therapeutic target for gastric cancer.
引用
收藏
页码：11979 / 11985
页数：7
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