Knockdown of Gab1 Inhibits Cellular Proliferation, Migration, and Invasion in Human Oral Squamous Carcinoma Cells

被引:12
|
作者
Xu, Luyong [1 ]
Li, Jie [1 ]
Kuang, Zheng [1 ]
Kuang, Yan [1 ]
Wu, Hong [1 ]
机构
[1] Jining Med Univ, Rizhao Peoples Hosp, Dept Stomatol, Taian Rd 126, Rizhao 276826, Peoples R China
关键词
Grb2-associated binder 1 (Gab1); Cdc20 homolog 1 (Cdh1); Malignance; Oral squamous cell carcinoma (OSCC); CANCER; EXPRESSION; APOPTOSIS; PATHWAY;
D O I
10.3727/096504017X15043589260618
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Grb2-associated binder 1 (Gab1) is often aberrant in cancerous cells and tissues, whose alteration is responsible for aggressive phenotypes. In this study, we examined the Gab1 expression in human oral Numinous cell carcinoma (OSCC) tissues and investigated the cellular and molecular effect of Gab1 on migration, invasion, and cell growth of the OSCC cell lines SCC15 and SCC25. We found that Gabl was overexpressed in OSCC tissues and cells, which is related to the protein levels of various molecules associated with cellular proliferation, migration, and invasion. Functional assays identified that Gabl overexpression promoted cell proliferation and invasion of OSCC cells and inhibited cell apoptosis in the SCC15 and SCC25 cell lines. On the other hand, Gab1 silencing affected the proliferation and invasion of OSCC cells and induced cell apoptosis. Western blot assay identified that Gabl overexpression suppressed the expression of Cdc20 homolog 1 (Cdh1) and then promoted cell invasion in OSCC cells. Furthermore. Gabl-mediated Cdhl downregulation was significantly reversed when the cells were subjected to an inhibitor of p-Akt. In conclusion, these results suggested that Gabl induced malignant progression of OSCC cells probably via activation of the Akt/Cdhl signaling pathway. Thus, Gabl may be a potential therapeutic target in the treatment of OSCC patients.
引用
收藏
页码:617 / 624
页数:8
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