Abstract
Triple-negative breast cancer (TNBC) has a poorer outcome than other subtypes of breast cancer, and the discovery of dysregulated microRNA (miRNA) and their role in tumor progression has provided a new avenue for elucidating the mechanism involved in TNBC. In this study, we identified that miR-3178 was significantly reduced in TNBC, and the low miR-3178 expression correlated with poor overall survival in TNBC but not in non-TNBC. The ectopic overexpression of miR-3178 suppressed TNBC cell proliferation, invasion, and migration by inhibiting the epithelial-to-mesenchymal (EMT) transition. Notch1 was validated as the direct target gene of miR-3178, which was confirmed by the dual-luciferase reporter assay. miR-3178 decreased the expression of Notch1 and restoration of Notch1 expression attenuated the inhibitory effects of miR-3178 on cell proliferation, metastasis, and the EMT in TNBC. miR-3178 inhibited cell proliferation and metastasis by targeting Notch1 in TNBC, and the restoration of miR-3178 might be a potential therapeutic strategy for TNBC.
Highlights
Triple-negative breast cancer (TNBC) represents an aggressive subtype of breast cancer characterized by lack of the estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2 (HER2)[1]
We showed that miR-3178 was downregulated in TNBC
To verify the differences in miR-3178 expression, we performed Quantitative real-time PCR (qRT-PCR) on 34 patient samples (17 with TNBC and 17 with non-TNBC), and found that miR-3178 was downregulated in TNBC (Fig. 1d)
Summary
Triple-negative breast cancer (TNBC) represents an aggressive subtype of breast cancer characterized by lack of the estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2 (HER2)[1]. This subtype of patient does not benefit from endocrine and anti-HER2 therapy. TNBC patients have a poorer prognosis than those with other subtypes of breast cancer[2,3]. This may be partly due to the inherently aggressive clinical behaviors and lack of proper therapeutic targets[2,4], as well as the high heterogeneity in genomics, epigenomics, transcriptomics, and proteomics that characterize TNBC molecular subtypes[5,6,7]. For better treatment of TNBC, there is an urgent need to further understand the
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