miR-520e regulates cell proliferation, apoptosis and migration in breast cancer

被引:20
作者
Yi, Ming [1 ,2 ]
Li, Minghua [1 ]
Long, Xia [1 ]
Ye, Jing [1 ]
Cui, Junwei [1 ]
Wei, Wei [1 ]
Wan, Huijuan [1 ]
Yin, Meijun [1 ]
Gao, Shuying [3 ]
Su, Zhengming [1 ,2 ]
Zhang, Fangting [1 ]
机构
[1] Peking Univ, Cent Lab, Shenzhen Hosp, Shenzhen 518036, Guangdong, Peoples R China
[2] Shantou Univ, Dept Grad Studies, Coll Med, Shantou 515041, Guangdong, Peoples R China
[3] Zunyi Med Univ, Dept Biochem & Mol Biol, Zhuhai Campus, Zhuhai 519041, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
miRNA-520e; proliferation; apoptosis; migration; breast cancer; MICRORNA; EXPRESSION; METASTASIS; INVASION; PROGRESSION; SIGNATURE; GENES;
D O I
10.3892/ol.2016.5085
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Previous studies have indicated that the deregulation of microRNAs contributes to tumorigenesis. Misregulation of microRNA-520e (miR-520e) has been observed in various types of cancer. However, the expression profile and biological function of miR-520e in breast cancer remains largely unknown. The present study demonstrated that miR-520e expression was significantly increased in breast cancer tissues compared with adjacent non-cancerous breast tissues in 21 patients, as revealed by reverse transcription-quantitative polymerase chain reaction. Furthermore, the proliferation capacity of breast cancer cells was markedly enhanced by the introduction of miR-520e in vitro using a cell counting kit-8 assay. The present study also revealed that the overexpression of miR-520e could suppress breast cancer cell apoptosis, revealed using Annexin V/propidium iodide double staining and flow cytometry analysis. In addition, the ectopic expression of miR-520e promoted the migration of breast cancer cells in vitro, as demonstrated by a Transwell assay. Overall, the findings of the present study highlight an important role for miR-520e in breast cancer development and in the molecular etiology of breast cancer, which indicates the potential application of miR-520e in cancer therapy.
引用
收藏
页码:3543 / 3548
页数:6
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