Abstract
Breast cancer (BC) is the most common cancer among women worldwide. However, there is insufficient research that focuses on the expression and molecular mechanisms of microRNA (miR)‑204‑5p in BC. In the current study, data were downloaded from the Cancer Genome Atlas (TCGA), the Gene Expression Omnibus (GEO) and the University of California Santa Cruz (UCSC) Xena databases. They were then used to undertake a meta‑analysis that leveraged the standard mean difference (SMD) and summarized receiver operating characteristic (sROC) to evaluate the expression of the precursor miR‑204 and mature miR‑204‑5p in BC. Additionally, an intersection of predicted genes, differentially expressed genes (DEGs) from the TCGA database and the GEO database were plotted to acquire desirable putative genes. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and protein‑protein interaction (PPI) network analyses were performed to assess the potential pathways and hub genes of miR‑204‑5p in BC. A decreased trend in precursor miR‑204 expression was detected in 1,077 BC tissue samples in comparison to 104 para‑carcinoma tissue samples in the TCGA database. Further, the expression of mature miR‑204‑5p was markedly downregulated in 756 BC tissue samples in comparison to 76 para‑carcinoma tissue samples in the UCSC Xena database. The outcome of the SMD from meta‑analysis also indicated that the expression of miR‑204‑5p was markedly reduced in 2,306 BC tissue samples in comparison to 367 para‑carcinoma tissue samples. Additionally, the ROC and sROC values indicated that miR‑204‑5p had a great discriminatory capacity for BC. In GO analysis, 'cell development', 'cell surface activity', and 'receptor agonist activity' were the most enriched terms; in KEGG analysis, 'endocytosis' was significantly enriched. Rac GTPase activating protein 1 (RACGAP1) was considered the hub gene in the PPI network. In conclusion, miR‑204‑5p may serve a suppressor role in the oncogenesis and advancement of BC, and miR‑204‑5p may have crucial functions in BC by targeting RACGAP1.