MiR-654-5p attenuates breast cancer progression by targeting EPSTI1

被引:3
|
作者
Tan, Yu-Yan [1 ,3 ]
Xu, Xiao-Yun [2 ]
Wang, Jin-Feng [1 ]
Zhang, Cheng-Wu [1 ]
Zhang, Sheng-Chu [1 ]
机构
[1] China Three Gorges Univ, Coll Clin Med Sci 1, Dept Gen Surg, 183 Yiling Ave, Yichang 443003, Hubei, Peoples R China
[2] China Three Gorges Univ, Coll Clin Med Sci 1, Dept Intens Care Unit, Yichang 443003, Hubei, Peoples R China
[3] Southeast Univ, Sch Med, Zhongda Hosp, Dept Gen Surg, Nanjing 210009, Jiangsu, Peoples R China
来源
AMERICAN JOURNAL OF CANCER RESEARCH | 2016年 / 6卷 / 02期
关键词
miRNA; breast cancer; miR-654-5p; EPSTI1; survival; EPITHELIAL-STROMAL INTERACTION; TUMOR-METASTASIS; IDENTIFICATION; MICRORNAS; INVASION; INSIGHTS;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
MicroRNAs (miRNAs) dysregulation is a common event in a variety of human diseases including breast cancer. However, clinical relevance and biological role of miR-654-5p in the progression of breast cancer remain greatly elusive. Herein, the expression levels of miR-654-5p were aberrantly downregulated in human breast cancer specimens and four breast cancer cell lines. Low expression of miR-654-5p was strongly associated with advanced TNM stage and lymph node metastasis as well as a poor survival. Functional analysis showed that miR-654-5p overexpression inhibited cell growth and invasion, and induced cell apoptosis in two aggressive breast cancer cells. Further studies demonstrated that Epithelial stromal interaction 1 (EPSTI1) was a direct target gene of miR-654-5p and showed an inverse correlation with miR-654-5p expression. Forced expression of EPSTI1 could abrogate the inhibitory effect of miR-654-5p on the growth and invasion of breast cancer cells as well as apoptosis-induced ability. In conclusion, the present study highlights that miR-654-5p acts as a tumor suppressor in breast cancer through directly targeting EPSTI1, and their functional regulation may open a novel avenue with regard to the therapeutic target for breast cancer.
引用
收藏
页码:522 / 532
页数:11
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