miR-365 overexpression promotes cell proliferation and invasion by targeting ADAMTS-1 in breast cancer

被引:31
作者
Li, Min [1 ]
Liu, Lulu [1 ]
Zang, Wenqiao [1 ]
Wang, Yuanyuan [1 ]
Du, Yuwen [1 ]
Chen, Xiaonan [1 ]
Li, Ping [2 ]
Li, Juan [2 ]
Zhao, Guoqiang [1 ]
机构
[1] Zhengzhou Univ, Coll Basic Med Sci, Zhengzhou 450001, Peoples R China
[2] Zhengzhou Univ, Affiliated Hosp 1, Dept Resp Med, Zhengzhou 450052, Peoples R China
基金
中国国家自然科学基金;
关键词
breast cancer; miR-365; cell cycle; invasion; ADAMTS-1; EXPRESSION; MICRORNAS; METASTASIS; DEREGULATION; BIOGENESIS; APOPTOSIS; GENES;
D O I
10.3892/ijo.2015.3015
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
MicroRNAs (miRNAs) have important roles in the initiation and progression of human cancer, including breast cancer. We evaluated miR-365 expression in breast cancer tissues, and investigated its effects on cell growth, cell cycle, cell invasion, and expression of its target gene ADAMTS-I. miR-365 expression levels were analyzed in breast cancer tissues and adjacent normal tissues using qRT-PCR. CCK-8, cell cycle, and invasion assays were used to explore the role of miR-365 expression in breast cancer cells. We conducted luciferase reporter and western blot assays to test whether ADAMTS-1 is a direct target of miR-365. We found that miR-365 expression levels were significantly higher in breast cancer tissues compared with adjacent non-tumor tissues (P<0.05). These relatively high expression levels were significantly associated with advanced clinical stages (P<0.05). In breast cancer cell lines, transfection with miR-365 inhibitor suppressed proliferation and invasion, and resulted in cell cycle arrest. Subsequent experiments indicated that miR-365 bound the 3'-UTR of ADAMTS-1 and downregulated its expression. Our findings indicated that the inhibition of miR-365 reduced cell proliferation and cell invasion. Additionally, miR-365 may function as a novel oncogene in breast cancer through targeting ADAMTS-1. These findings provide insight into the mechanism of breast cancer pathogenesis.
引用
收藏
页码:296 / 302
页数:7
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