Effect of silencing SATB1 on proliferation, invasion and apoptosis of A549 human lung adenocarcinoma cells

被引:12
作者
Huang, Bo [1 ]
Zhou, Hongli [2 ]
Wang, Siwang [1 ]
Lang, Xian Ping [1 ]
Wang, Xiaodong [1 ]
机构
[1] Liaoning Med Univ, Dept Thorac Surg, Affiliated Hosp 1, 2 People St, Jinzhou 121000, Liaoning, Peoples R China
[2] Liaoning Med Univ, Dept Kidney Dis, Affiliated Hosp 1, Jinzhou 121000, Liaoning, Peoples R China
关键词
lung cancer; siRNA; special adenine-thymine-rich sequence-binding protein 1; ORGANIZER SATB1; GENE-EXPRESSION; CANCER; METASTASIS; GROWTH;
D O I
10.3892/ol.2016.5179
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The present study aimed to explore the clinical characteristics of special adenine-thymine-rich sequence-binding protein 1 (SATB1) in lung adenocarcinoma and its role in the proliferation, invasion, migration and apoptosis of the lung adenocarcinoma cell line A549. The expression of SATB1 was first studied in tumor tissues of lung adenocarcinoma and adjacent non-tumor tissues. The siRNA green fluorescent protein expression vector of SATB1 was constructed and transfected into the lung adenocarcinoma cell line A549, then a fluorescence microscope was used to study the transfection efficiency. Western blot analysis was adopted to measure the silencing efficiency. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), Transwell and scratch assays were used to study cell proliferation, invasion and migration activity, and the apoptosis rate was tested by flow cytometry. SATB1 expression was low in the adjacent non-tumor tissues but high in lung adenocarcinoma tissues, and it was reversely proportional to the differentiation degree. Following transfection with SATB1-siRNA, the expression of SATB1 in A549 cells was blocked (P<0.01). In addition, the proliferation, invasion and migration abilities of cells decreased significantly while the apoptosis rate increased significantly (P<0.01). In conclusion SATB1 is closely associated with the pathogenesis and development of lung adenocarcinoma.
引用
收藏
页码:3818 / 3824
页数:7
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