Cargando…

MicroRNA-589 serves as a tumor suppressor microRNA through directly targeting metastasis-associated protein 2 in breast cancer

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 reve...

Descripción completa

Detalles Bibliográficos
Autor principal: Chu, Jun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6676663/
https://www.ncbi.nlm.nih.gov/pubmed/31452724
http://dx.doi.org/10.3892/ol.2019.10548
Descripción
Sumario: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.