English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

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.

miR‑185‑5p inhibits F‑actin polymerization and reverses epithelial mesenchymal transition of human breast cancer cells by modulating RAGE