miR-17-5p suppresses cell proliferation and invasion by targeting ETV1 in triple-negative breast cancer

作者：Jie Li, Yuanhui Lai, Jieyi Ma, Yue Liu, Jiong Bi, Longjuan Zhang, Lianzhou Chen, Yao Chen, Weiming Lv, Guangqi Chang, Shenming Wang, Mao Ouyang, Wenjian Wang · 发表于：BMC Cancer · 年份：2017 · DOI：10.1186/s12885-017-3674-x · 被引用次数：127 · 研究领域：MicroRNA in disease regulation、Circular RNAs in diseases、Kruppel-like factors research

Triple-negative breast cancer (TNBC) is the malignancy with the worst outcome among all breast cancer subtypes. We reported that ETV1 is a significant oncogene in TNBC tumourigenesis. Consequently, investigating the critical regulatory microRNAs (miRNAs) of ETV1 may be beneficial for TNBC targeted therapy. We performed in situ hybridization (ISH) and immunohistochemistry (IHC) to detect the location of miR-17-5p and ETV1 in TNBC patient samples, respectively. miR-17-5p expression in TNBC tissues and cell lines was assessed by quantitative real-time PCR (qRT-PCR). ETV1 expression was evaluated by qRT-PCR, western blotting and IHC. Cell Counting Kit-8 (CCK-8), colony formation, Transwell and wound closure assays were utilized to determine the TNBC cell proliferation and migration capabilities. In vivo tumour metastatic assays were performed in a zebra fish model. The abundance of miR-17-5p was significantly decreased in TNBC cell lines and clinical TNBC tissues. The miR-17-5p expression levels were closely correlated with tumour size ( P < 0.05) and TNM stage ( P < 0.05). By contrast, the expression of ETV1 was significantly up-regulated in TNBC cell lines and tissues. There is an inverse correlation between the expression status of miR-17-5p and ETV1 ( r = −0.28, P = 3.88 × 10 −3 ). Luciferase reporter assay confirmed that ETV1 was a direct target of miR-17-5p. Forced expression of miR-17-5p in MDA-MB-231 or BT549 cells significantly decreased ETV1 expression and suppressed ce...