MicroRNA‑589 serves as a tumor suppressor microRNA through directly targeting metastasis‑associated protein 2 in breast cancer
Published online on: June 28, 2019
Copyright: © Chu et al.
This is an open access article distributed under the terms of Creative Commons Attribution License.
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Triple‑negative breast cancer (TNBC) has a poorer outcome compared with that of 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. Previous studies have revealed that aberrant expression of miRNA‑589 (miR‑589) was frequently observed in various types of cancer. However, the expression and function of miR‑589 in TNBC has not been well illustrated. In the present study, the expression level of miR‑589 was explored in TNBC tissues and TNBC cell lines by quantitative polymerase chain reaction (qPCR). The results revealed that the expression of miR‑589 was decreased in TNBC tissues and cell lines compared with that in normal tissues and breast cell lines. Furthermore, miR‑589 overexpression decreased the TNBC cell proliferation, migration and invasion, whereas miR‑589 silencing generated the opposite results in vitro. Bioinformatic algorithms predicted a direct target site for miR‑589 in the 3'‑untranslated region of metastasis‑associated protein 2 (MTA2), which was confirmed with a dual‑luciferase reporter assay and western blot analysis. Results of the qPCR and western blot analysis illustrated that miR‑589 negatively regulated MTA2 expression with regard to mRNA and protein levels in the TNBC cell lines. MTA2 silencing reversed the promotion function of miR‑589 inhibitor in the TNBC cell line. Finally, miR‑589 could inhibit the process of epithelial‑mesenchymal transition via MTA2. In summary, the present study revealed the biological function and molecular mechanism of miR‑589 in the progression of TNBC. MiR‑589 inhibition in the progression of TNBC may be a potential therapeutic target for TNBC.