Promotion of the Proliferation and Migration of Breast Cancer Cells by the Micro Ribonucleic Acid miR-425-5p via Dihydropyrimidinase-Like 2

Breast cancer (BC) is the most common malignant tumor in women. MicroRNAs (miRNAs) are a class of noncoding single-stranded RNA molecules that are closely related to the development, progression, and metastasis of BC. The miRNA miR-425-5p is upregulated in a variety of cancers and can promote cancer progression. This study aimed to investigate the role of miR-425-5p in BC and its molecular mechanism. The expression of miR-425-5p in BC was analyzed using the Cancer Genome Atlas database and two Gene Expression Omnibus validation cohorts. Expression of miR-425-5p in paired BC and adjacent nontumor tissues from four patients with invasive ductal carcinoma and in normal breast epithelial and BC cell lines. Expression of miR-425-5p in BC tissues and cell lines was detected via quantitative real-time polymerase chain reaction. Protein expression was detected using a Western blot. Cell growth and proliferation were assessed via a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. A transwell assay was used to detect the migration ability of BC cells. The effects of miR-425-5p and DPYSL2 were verified using patient-derived BC organoids established from the four tumor samples, as well as xenograft experiments in female nude mice randomly divided into three groups (five or eight mice per group). The experimental results showed that miR-425-5p expression levels were higher in tumor tissue than in normal tissue. The RT-qPCR results showed high expression of miR-425-5p in clinical samples and BC cell lines; miR-425-5p promoted the growth and migration of BC cells and targeted and degraded the DPYSL2 messenger RNA. The DPYSL2 protein content decreased upon miR-425-5p overexpression. The MTT and Transwell assay results indicated that miR-425-5p regulated BC progression via DPYSL2. Inhibition of miR-425-5p or overexpression of DPYSL2 inhibited BC growth in organoid and nude mouse xenograft experiments. In summary, miR-425-5p promoted BC development by targeting DPYSL2.