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MiR-3178 inhibits cell proliferation and metastasis by targeting Notch1 in triple-negative breast cancer.


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.

SUBMITTER: Kong P 

PROVIDER: S-EPMC6192997 | biostudies-other | 2018 Oct

REPOSITORIES: biostudies-other

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miR-3178 inhibits cell proliferation and metastasis by targeting Notch1 in triple-negative breast cancer.

Kong Peng P   Chen Lie L   Yu Muxin M   Tao Jing J   Liu Jiawei J   Wang Yue Y   Pan Hong H   Zhou Wenbin W   Wang Shui S  

Cell death & disease 20181017 11


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 prolif  ...[more]

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