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Involvement of NEDD9 in the invasion and migration of gastric cancer

波形蛋白 基因敲除 癌基因 下调和上调 免疫印迹 细胞迁移 癌症研究 转染 MTT法 生物 细胞培养 细胞生长 细胞 免疫组织化学 分子生物学 细胞周期 免疫学 生物化学 基因 遗传学
作者
Feng Jin,Jinpeng Zhao,Haibin Xie,Yong Yin,Guanghua Luo,Jun Zhang,Yuehua Feng,Li Zhong
出处
期刊:Tumor Biology [SAGE Publishing]
卷期号:36 (5): 3621-3628 被引量:14
标识
DOI:10.1007/s13277-014-2999-1
摘要

Recent studies have demonstrated that neural precursor cell expressed, developmentally downregulated 9 (NEDD9) is highly expressed in various tumor tissues and cell lines. However, research on the role of NEDD9 in gastric cancer (GC) is rare, and the potential mechanism in tumor progression has not yet been explored. In this study, we investigated the role and mechanism of NEDD9 in GC. The expression of NEDD9 in GC tissues and cell lines was measured by immunohistochemistry, qRT-PCR, and Western blot, respectively. Inhibiting NEDD9 expression was carried out by siRNA transfection, and upregulating of NEDD9 was via NEDD9 overexpression plasmid. The ability of proliferation, migration, and invasion was detected by MTT assay, scratch wound assay, and transwell assay, respectively. The expression of vimentin, E-cadherin, Zeb1, and Zeb2 was measured by Western blot and qRT-PCR. We found that NEDD9 expression was dramatically increased both in GC tissues and cell lines, and the expression was significantly related to GC development. Knockdown of NEDD9 in SGC-7901 strongly inhibited its malignant capacity in vitro. Meanwhile, upregulation of NEDD9 in GES-1 increased the malignant capacity. In addition, the expression of vimentin, Zeb1, and Zeb2 was positively correlated with NEDD9, while E-cadherin was opposite. Collectively, our findings suggest that NEDD9 acts as an oncogene and promotes GC metastasis via EMT.
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