Reciprocal regulation of Hsa-miR-1 and long noncoding RNA MALAT1 promotes triple-negative breast cancer development

被引:106
|
作者
Jin, Chuan [1 ]
Yan, Bingchuan [1 ]
Lu, Qin [1 ]
Lin, Yanmin [2 ]
Ma, Lei [1 ]
机构
[1] Guangzhou Med Univ, Affiliated Canc Hosp, Guangzhou, Guangdong, Peoples R China
[2] Guangdong Med Coll, Affiliated Hosp, Ctr Oncol, Zhanjiang, Peoples R China
关键词
miR-1; Slug; MALAT1; Triple-negative breast cancer; LUNG-CANCER; METASTASIS; MICRORNAS; EXPRESSION; CELLS; CARCINOMA; PROLIFERATION; MUTATIONS; PROGNOSIS; APOPTOSIS;
D O I
10.1007/s13277-015-4605-6
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Recent studies demonstrated that long noncoding RNAs (lncRNAs) have a critical role in the regulation of cancer progression and metastasis. However, little is known about the mechanism through which metastasis-associated lung adencarcinoma transcript 1 (MALAT1) exerts its oncogenic activity, and the interaction between MALAT1 and microRNA remains largely unknown. In the present study, we reported that MALAT1 was upregulated in triple-negative breast cancer (TNBC) tissues. Knockdown of MALAT1 inhibited proliferation, motility, and increased apoptosis in vitro. In vivo study indicated that knockdown of MALAT1 inhibited tumor growth and metastasis. Patients with high MALAT1 expression had poorer overall survival time than those with low MALAT1 expression. In addition, our findings demonstrate a reciprocal negative control relationship between MALAT1 and miR-1: downregulation of MALAT1 increased expression of microRNA-1 (miR-1), while overexpression of miR-1 decreased MALAT1 expression. Slug was identified as a direct target of miR-1. We proposed that MALAT1 exerted its function through the miR-1/slug axis. In summary, we proposed that MALAT1 may be a target for TNBC therapy.
引用
收藏
页码:7383 / 7394
页数:12
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