Conclusions
Collectively, our results revealed 18 upregulated genes in TNBC. Notably, CDK1 and its related microRNA miR-143-3p could be potential therapeutic targets for TNBC.
Methods
We screened the Gene Expression Omnibus database for transcriptome data and identified differently expressed genes in TNBC. Then, we performed Gene Ontology analysis to determine the genes and pathways involved in TNBC development. We correlated significantly expressed genes and miRNAs using miRDB, TargetScan, miRWalk, and DIANA, and then validated the expression of CDK1 and miR-143-3p in TNBC patients.
Objective
Triple-negative breast cancer (TNBC) is characterized by a lack of targeted therapies and poor patient prognosis, and its underlying pathological mechanisms remain unclear. This study aimed to identify potential key genes and related pathways that are required for TNBC development.
Results
Eighteen genes were significantly upregulated in TNBC patients, and these were found to be enriched in cell metabolic process, cell division, mitochondrion, and respiratory chain. MiR-143-3p was found to be an upstream regulator of CDK1. Validation experiments revealed that CDK1 was upregulated while miR-143-3p was downregulated in clinical TNBC specimens. Conclusions: Collectively, our results revealed 18 upregulated genes in TNBC. Notably, CDK1 and its related microRNA miR-143-3p could be potential therapeutic targets for TNBC.