Akademik Veri Yönetim Sistemi
Turkish Journal of Biochemistry, 2025 (SCI-Expanded, Scopus, TRDizin)
Hepatocellular carcinoma (HCC) and sepsis are significant global health challenges, both involving complex molecular mechanisms that may overlap. Identifying shared differentially expressed genes (DEGs) between these conditions could provide novel insights into disease progression and therapeutic targets. This study aimed to determine common DEGs between HCC and sepsis using microarray datasets and to explore their biological implications through bioinformatics analyses. Publicly available microarray datasets for HCC and sepsis were retrieved from gene expression repositories. After preprocessing and normalization, DEGs were identified using statistical approaches, and overlapping genes were determined through comparative analysis. Functional enrichment analysis was performed with the DAVID platform to assess associated biological processes and pathways. A protein-protein interaction (PPI) network was then constructed to identify hub genes, and transcription factor (TF)-gene interaction analysis was carried out to evaluate potential regulatory mechanisms shared between the two conditions. A total of 379 common DEGs were identified between HCC and sepsis. Functional enrichment analysis indicated that these DEGs were mainly related to immune response, cell cycle regulation, and antigen presentation pathways. PPI network analysis revealed hub genes including CCNA2, NUSAP1, TOP2A, and CDK1, all of which were significantly upregulated in both diseases. TF-gene interaction analysis highlighted convergent transcriptional regulatory mechanisms linking immune dysregulation in sepsis with tumorigenesis in HCC. This study demonstrates molecular similarities between HCC and sepsis, emphasizing shared DEGs and regulatory networks. The identification of hub genes and enriched pathways provides potential diagnostic markers and therapeutic targets, underscoring the importance of transcriptional dysregulation in both cancer development and sepsis pathophysiology.