Cargando…
miR-185-5p inhibits F-actin polymerization and reverses epithelial mesenchymal transition of human breast cancer cells by modulating RAGE
In our previous study, advanced glycosylation end-product specific receptor (RAGE) was observed to bind to S100A8/A9 and cause epithelial mesenchymal transition (EMT). The results from target gene prediction revealed that microRNA (miR)-185-5p had a RAGE binding site. However, the function of miR-18...
Autores principales: | , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6102692/ https://www.ncbi.nlm.nih.gov/pubmed/30015912 http://dx.doi.org/10.3892/mmr.2018.9294 |
Sumario: | In our previous study, advanced glycosylation end-product specific receptor (RAGE) was observed to bind to S100A8/A9 and cause epithelial mesenchymal transition (EMT). The results from target gene prediction revealed that microRNA (miR)-185-5p had a RAGE binding site. However, the function of miR-185-5p in the invasion and migration of breast cancer remains ambiguous. In the present study, the expression of miR-185-5p was examined in breast cancer tissues and cells. Clinical features revealed a negative correlation between miR-185-5p and tumor size, as well as in tumor differentiation and lymph node metastasis in breast cancer. In addition, miR-185-5p was negatively associated with RAGE, and this miRNA reversed the EMT of breast cancer by modulating RAGE in vitro. In addition, miR-185-5p inhibited the S100A8/A9-induced EMT of breast cancer cells by the nuclear factor-κB/Snail signaling pathway. Notably, miR-185-5p upregulation inhibited the F-actin polymerization induced by S100A8/A9 in breast cancer. Furthermore, overexpression of miR-185-5p and reduction of RAGE inhibited lung metastasis node in vivo. Thus, miR-185-5p represents a potential therapeutic target in breast cancer by modulating RAGE. |
---|