Identification of EDNRA as the Key Biomarker for Hypercholesterolemia and Colorectal Cancer.
Tohoku J Exp Med
; 262(3): 181-189, 2024 Mar 15.
Article
en En
| MEDLINE
| ID: mdl-38123303
ABSTRACT
Some studies have investigated the role of cholesterol in the progression of colorectal cancer (CRC). However, the underlying mechanism of action is not clear. In this study, we used bioinformatics tools to elucidate the molecular mechanisms involved. We initially obtained CRC datasets from the Gene Expression Omnibus (GEO) database and hypercholesterolemia data from GeneCards and DisGeNE. Common differentially expressed genes (DEGs) were determined by using Venn diagram web tools. Next, we performed Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses using the Database for Annotation, Visualization, and Integrated Discovery (DAVID). The hub gene was identified through common expression pattern analysis and survival analysis. Finally, we conducted an immune regulatory point analysis and predicted target drugs based on the hub gene. The results of our analysis revealed 13 common DEGs, with endothelin receptor type A (EDNRA) identified as the hub gene linking hypercholesterolemia and CRC. The results of the GO analysis showed that the common DEGs were primarily associated with the G-protein coupled receptor signaling pathway, extracellular space, and receptor binding. The results of the KEGG pathway enrichment analysis indicated enrichment in pathways related to cancer and the phospholipase D signaling pathway. Additionally, we identified potential target drugs, including Podocarpus montanus, Diospyros kaki, Herba Salviae japoniae, sitaxentan, and ambrisentan. We found that EDNRA might be an underlying biomarker for both hypercholesterolemia and CRC. The predicted target drugs provide new strategies for treating CRC.
Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Neoplasias Colorrectales
/
Hipercolesterolemia
Límite:
Humans
Idioma:
En
Revista:
Tohoku J Exp Med
Año:
2024
Tipo del documento:
Article