Identification of Critical Hub Genes and Pathways Regulating Chemotherapy Responses in Triple-Negative Breast Cancer:...

Triple-negative breast cancer (TNBC) signifies an enormous risk to women's health globally. TNBC is characterized by its aggressive nature, resistance to existing therapies, and poor prognosis. Understanding the molecular pathogenesis of breast cancer is crucial for identifying screening markers and therapeutic targets. In order to find commonly expressed differentially expressed genes (DEGs) in a variety of TNBC cell lines treated with docetaxel (GSE70690), paclitaxel (GSE86839), doxorubicin (GSE202536), and cisplatin (GSE77515), as well as untreated TNBC cell lines (GSE38959), bioinformatics approaches were used. The R software was utilized, and the cutoff criteria for the analysis were set at p < 0.01 and |log2FC| > ±1. A Venn diagram was used to identify the shared DEGs across TNBC cell lines treated with and without the targeted chemotherapeutic drugs. The DEGs that were found were analyzed to determine their involvement in specific biological processes and pathways using gene ontology and Reactome pathway enrichment analysis. Protein-protein interactions (PPI) were subsequently established, and the hub genes were discovered. Through data analysis, the study identified a set of DEGs associated with the response to chemotherapy drugs in TNBC. The GO analysis revealed that the DEGs identified were primarily associated with cell cycle regulation, cell population proliferation, and microtubule-related functions. Reactome pathway analysis showed enrichment in cell cycle processes, mitotic phases, and DNA damage checkpoints. Hub genes, such as CDK2, PLK4, and BIRC5, were identified based on their high degree of connectivity in the PPI network. The identified DEGs and pathways in this study shed light on possible therapeutic targets and reducing drug resistance. These findings contribute to the development of personalized and targeted therapies for TNBC, ultimately leading to improved patient outcomes.