miR-381 inhibited breast cancer cells proliferation, epithelial-to-mesenchymal transition and metastasis by targeting CXCR4

被引:74
作者
Xue, Yubao [1 ]
Xu, Wenjing [2 ]
Zhao, Wei [3 ]
Wang, Wei [4 ]
Zhang, Dahong [5 ]
Wu, Ping [6 ]
机构
[1] Xuzhou Med Univ, Huaian Hosp, Dept Oncol, Huaian 223002, Peoples R China
[2] Huaiyin Hosp Huaian City, Dept Lab, Huaian 223300, Peoples R China
[3] Nanjing Matern & Child Hlth Care Hosp, Dept Lab, Nanjing 210000, Jiangsu, Peoples R China
[4] Nanjing Matern & Child Hlth Care Hosp, Dept Pathol, Nanjing 210000, Jiangsu, Peoples R China
[5] Nanjing Med Unvers, Huaan Peoples Hosp 1, Dept Oncol, Huaian 223300, Peoples R China
[6] Huaian Matern & Child Hlth Care Hosp, Dept Pathol, Huaian 223002, Peoples R China
关键词
miR-381; Breast cancer; CXCR4; Proliferation; EMT; Metastasis; CHEMOKINE RECEPTOR CXCR4; PROSTATE-CANCER; DOWN-REGULATION; TUMOR-SUPPRESSOR; MIR-200; FAMILY; E-CADHERIN; EXPRESSION; INVASION; EMT; PROGRESSION;
D O I
10.1016/j.biopha.2016.12.051
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Background: MicroRNAs act as posttranscriptional regulators of gene expression in many biological processes, which played a vital role in regulation cancer cells epithelial-to-mesenchymal transition and metastasis. The deregulation of miR-381 has been identified in breast cancer. However, the role and mechanism of miR-381 in breast cancer have not been completely unexplored. Methods: Total RNA was extracted from the tissues of 27 patients with breast cancer and two breast cancer cell lines, respectively. The expression levels of miR-381 were examined by quantitative real-time PCR. The stable overexpress or silence miR-381 expression cells lines and control cells line were constructed by lentivirus infection. Subsequently, cell proliferation, cell migration, invasion assay and western blot assay were performed to detect the biological functions of miR-381 in vitro. Moreover, a luciferase reporter assay was conducted to confirm target associations. Results: In this study, we validated the lower expression of miR-381 in breast cancer tissues than their adjacent non-neoplastic tissues in 27 breast cancer patients. The result also showed that miR-381 was lowly expressed in breast cancer cell lines MCF-7 and MDA-MB-231 than human epithelial cell line MCF-10A. The miR-381 expression was significantly up-regulated under exogenous miRNA-381 treatment in MCF-7 and MDA-MB-231 cells analyzed by quantitative real-time PCR. The results also indicated that an inverse correlation existed between miR-381 expression level and breast cancer cell proliferation, epithelial-to-mesenchymal transition and metastasis. Furthermore, miR-381 was predicted as a regulatory miRNA of CXCR4 in breast cancer, and the data analysis revealed that there was a negatively relationship between miR-381 and CXCR4 expression in breast cancer tissues from the patients. miR-381 played an important role in breast cancer cells proliferation, epithelial-tomesenchymal transition and metastasis by targeting CXCR4. Conclusions: This present study revealed that miR-381 might be considered as a novel therapeutic target for breast cancer treatment. (C) 2016 Elsevier Masson SAS. All rights reserved.
引用
收藏
页码:426 / 433
页数:8
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