siRNA-induced ABCE1 silencing inhibits proliferation and invasion of breast cancer cells

被引:34
作者
Huang, Bo [1 ]
Zhou, Hongli [2 ]
Lang, Xianping [1 ]
Liu, Zhiliang [1 ]
机构
[1] Liaoning Med Univ, Affiliated Hosp 1, Dept Thorac Surg, Jinzhou 121000, Liaoning, Peoples R China
[2] Liaoning Med Univ, Affiliated Hosp 1, Dept Urol, Jinzhou 121000, Liaoning, Peoples R China
基金
中国国家自然科学基金;
关键词
breast cancer; siRNA; ABCE1; RNASE-L; LUNG-CANCER; EXPRESSION; ROLES; GENE;
D O I
10.3892/mmr.2014.2424
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Breast cancer is the most common type of cancer among females and the adenosine triphosphate (ATP) binding cassette E1 (ABCE1) gene is a member of the ATP-binding cassette (ABC) family. Studies in lung cancer have shown that overexpression of ABCE1 in tumor cells promotes growth and inhibits apoptosis. However, little is known about whether the ABCE1 gene is associated with breast cancer. In the present study, ABCE1 expression was assessed in breast cancer tissue and adjacent normal breast tissue using immunohistochemistry. Furthermore, small interfering (si)RNA targeting ABCE1 was constructed and transfected into MCF-7 human breast cancer cells to downregulate ABCE1 expression. The effect of ABCE1 knockdown on cell proliferation, invasion, apoptosis and gene expression was then assessed using MTT assay, Transwell migration assay, flow cytometry and western blot analysis, respectively. ABCE1 was observed to be overexpressed in breast cancer tissue compared with adjacent normal breast tissue. Furthermore, ABCE1-siRNA was found to inhibit proliferation and invasion in breast cancer cells, significantly induce breast cancer cell apoptosis (P<0.05) in vitro and increase the protein expression of RNase L. These findings showed that ABCE1 had an important role in proliferation, invasion and apoptosis in MCF-7 human breast cancer cells and that ABCE1 may inhibit intracellular RNase L activity, which inhibits the 2-5A/RNase L pathway, interfering with the biological characteristics of breast cancer cells.
引用
收藏
页码:1685 / 1690
页数:6
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