Identification of hub genes and pathways in hepatitis B virus-associated hepatocellular carcinoma: A comprehensive in silico study.
Health Sci Rep
; 7(6): e2185, 2024 Jun.
Article
em En
| MEDLINE
| ID: mdl-38895552
ABSTRACT
Background and Aim:
The hepatitis B virus (HBV) is one of the most common causes of liver cancer in the world. This study aims to provide a better understanding of the mechanisms involved in the development and progression of HBV-associated hepatocellular carcinoma (HCC) by identifying hub genes and the pathways related to their functions.Methods:
GSE83148 and GSE94660 were selected from the Gene Expression Omnibus (GEO) database, differentially expressed genes (DEGs) with an adjusted p-value < 0.05 and a |logFC| ≥1 were identified. Common DEGs of two data sets were identified using the GEO2R tool. The Kyoto Encyclopedia of Genes and Genomes (KEGG) and gene ontology (GO) databases were used to identify pathways. Protein-protein interactions (PPIs) analysis was performed by using the Cytoscap and Gephi. A Gene Expression Profiling Interactive Analysis (GEPIA) analysis was carried out to confirm the target genes.Results:
One hundred and ninety-eight common DEGs and 49 hub genes have been identified through the use of GEO and PPI, respectively. The GO and KEGG pathways analysis showed DEGs were enriched in the G1/S transition of cell cycle mitotic, cell cycle, spindle, and extracellular matrix structural constituent. The expression of four genes (TOP2A, CDK1, CCNA2, and CCNB2) with high scores in module 1 were more in tumor samples and have been identified by GEPIA analysis.Conclusion:
In this study, the hub genes and their related pathways involved in the development of HBV-associated HCC were identified. These genes, as potential diagnostic biomarkers, may provide a potent opportunity to detect HBV-associated HCC at the earliest stages, resulting in a more effective treatment.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Idioma:
En
Revista:
Health Sci Rep
Ano de publicação:
2024
Tipo de documento:
Article