MiR-508-3p inhibits cell invasion and epithelial-mesenchymal transition by targeting ZEB1 in triple-negative breast cancer

S.-J. Guo, H.-X. Zeng, P. Huang, S. Wang, C.-H. Xie, S.-J. Li

Department of Internal Medicine, Ganzhou Cancer Hospital, Ganzhou, Jiangxi, P.R. China. jiang59daoketanwu@163.com

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• Oncology

OBJECTIVE: Recently, studies have identified that microRNAs (miRNAs) are novel regulators for gene expression in tumor progression including breast cancer. The aim of the study is to investigate the clinical significance and underlying functions between miR-508-3p expression and triple-negative breast cancer (TNBC) development.

PATIENTS AND METHODS: Quantitative Real-time PCR (QRT-PCR) was performed to determine the expression of miR-508-3p in 54 pairs of TNBC specimens and adjacent non-tumor tissues. The association between miR-508-3p expression and clinicopathological factors was assessed using x2-test. Transwell invasion assays were used to assess cell invasion ability. Luciferase reporter assay, Western blot analyses and qRT-PCR were performed to demonstrate ZEB1 was a direct target of miR-508-3p.

RESULTS: We demonstrated that miR-508-3p expression was remarkably decreased in TNBC tissues and cells. Lower miR-508-3p expression significantly associated with lymph node metastasis and distant metastasis in TNBC patients (p < 0.05). Ectopic expression of miR-508-3p significantly suppressed cell invasion ability of TNBC. MiR-508-3p overexpression suppressed cell epithelial-mesenchymal transition (EMT) phenomenon of TNBC by upregulating E-cadherin expression, but downregulating Vimentin expression. In addition, we revealed that ZEB1 was a direct target of miR-508-3p in TNBC cells. MiR-508-3p significantly suppressed cell EMT process by regulating ZEB1 expression.

CONCLUSIONS: We found that miR-508-3p may be a potential therapeutic target of TNBC.

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