With the consideration of the dynamic role of
microRNAs (
miRNAs) in
breast cancer,
miRNAs may serve as therapeutic targets, helping to prevent development of
therapy resistance, maintain stable disease, and prohibit metastatic spread. We identified the differentially expressed
breast cancer-related gene
ribonucleotide reductase subunit M2 (RRM2) as the study focus through microarray expression profiles. Next, the upstream regulatory
microRNA (miR)-4500 of RRM2 was predicted using bioinformatics website analysis, and their binding was verified by a dual
luciferase reporter gene assay. The regulatory effects of miR-4500 on
breast cancer cell proliferation, apoptosis, migration, invasion, and capillary-like tube formation of endothelial cells were assessed by gain- and loss-of-function experiments. The experimental data revealed that miR-4500 was downregulated, whereas RRM2 was upregulated in
breast cancer cells. Mechanistic analysis revealed that miR-4500 downregulated the RRM2 expression to inactivate the
mitogen-activated protein kinase (MAPK) signaling pathway. Furthermore, miR-4500 exerted anti-
tumor effects by targeting RRM2 through suppression of the MAPK signaling pathway in vitro, evidenced by attenuated
cancer cell migration and invasion and capillary-like tube formation of endothelial cells. The in vivo experiments further corroborated in vitro results. Collectively, overexpressed miR-4500 could downregulate RRM2 and inhibit activation of the MAPK signaling pathway, thus attenuating
breast cancer cell proliferation, invasion, migration, and angiogenesis and promoting
breast cancer cell apoptosis.