Screening and biological function analysis of differentially expressed genes associated with miR-21 in hepatocellular carcinoma tissue
Abstract
Objective To investigate the differentially expressed genes (DEGs) associated with miR-21 between hepatocellular carcinoma (HCC) tissue and normal tissue, as well as their biological function in the development and progression of HCC. Methods The GSE65892 dataset with good data integrity was obtained from the GEO database. GEO2R tool was used to import data into R language, and the limma package was used to identify miR-21-related DEGs. DAVID database was used to perform gene ontology (GO) functional annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses of miR-21-related DEGs. A protein-protein interaction (PPI) network was constructed for miR-21-related DEGs to identify hub genes, and the Kaplan-Meier survival curve was used to investigate the value of these hub genes in predicting the prognosis of HCC patients. Results A total of 74 miR-21-related DEGs were identified in the GSE65892 dataset, with 23 upregulated genes and 51 downregulated genes. The GO functional annotation and KEGG pathway enrichment analyses showed that these DEGs were involved in the biological processes such as cellular response to lipopolysaccharide and angiogenesis. The PPI network analysis identified 18 downregulated and 2 upregulated hub genes, and the survival analysis showed that 8 hub genes (RBM12, HNRNPD, CXCL8, TRA2A, DDIT3, RPS24, LRRC57, and CXCL2) were significantly associated with poor prognosis in HCC patients. Conclusion RBM12, HNRNPD, CXCL8, TRA2A, DDIT3, RPS24, LRRC57, and CXCL2 are the miR-21-related DEGs that are significantly associated with poor prognosis of patients. These genes participate in the development and progression of HCC by regulating immune function and cell differentiation, proliferation, and apoptosis.
Fields of Study & Subjects
Ferroptosis and cancer prognosis
MicroRNA in disease regulation
Cancer-related molecular mechanisms research
Publication details
- Journal / source
- DOAJ (DOAJ: Directory of Open Access Journals)
- Publication date
- 1 February 2026
- Language
- ZH