Analysis of expression profile data identifies key genes and pathways in hepatocellular carcinoma

Abstract

Abstract. The aims of the present study were to identify key genes and pathways associated with hepatocellular carcinoma (HCC) progression and predict compounds potentially associated with this type of carcinogenesis. The gene expression profile data of the GSE49515 dataset was obtained from the Gene Expression Omnibus database. The limma software package was used to identify the differentially expressed genes (DEGs). Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed using the Biological Networks Gene Ontology tool and the Database for Annotation, Visualization and Integrated Discovery, respectively. The Michigan Molecular Interactions database plugin within the Cytoscape software platform was used to perform protein-protein interaction (PPI) network analysis. Chemical-gene interaction data for HCC were obtained from the Comparative Toxicogenomics Database to evaluate the associations between drugs and specific genes. A total of 302 DEGs, including 231 downregulated and 71 upregulated, were identified. Cytokine-cytokine receptor interaction and chemokine signaling were the significantly enriched pathways. Additionally, PPI network analysis indicated a total of 13 highest degree hub nodes, including FBJ murine osteosarcoma viral oncogene homolog (FOS) and DNA damage-inducible transcript 3 protein (DDIT3). Chemical-gene interaction analysis revealed that FUN and FOS were targeted by >500 compounds, while >200 genes were targeted by 2,3,7,8-tetrachlorodibenzodioxin and benzo(α)pyrene. In conclusion, the present study demonstrated that FOS, DDIT3, the cytokine-cytokine receptor interaction pathway and the chemokine signaling pathway may be key genes and pathways associated with the development of HCC. Furthermore, exposure to 2,3,7,8-tetrachlorodibenzodioxin or benzo(α)pyrene may lead to hepatocarcinogenesis.

An immune-related gene signature for predicting survival and immunotherapy efficacy in hepatocellular carcinoma

“…A total of 329 DEIRGs were identi ed, of which the most relevant biological process and signaling pathway was "immune response" and "cytokine-cytokine receptor interaction", respectively. This result was closely associated with immune, which was consistent with some existing literature reports [43]. Subsequently, Cox regression analysis and LASSO regression model identi ed 11 out of 81 prognosis-related IRGs, which were used to construct IRGPI, including NDRG1, FABP6, MAPT, HSP90AA1, CD320, CACYBP, BRD8, OSGIN1, NRAS, ISG20L2, and PSMD14.…”

1,8 Cineole and Ellagic acid inhibit hepatocarcinogenesis via upregulation of MiR-122 and suppression of TGF-β1, FSCN1, Vimentin, VEGF, and MMP-9

“…Studies proved that hepatocarcinogenesis had been linked with variations in several important cellular responses. Targeting molecules during the multistep process of hepatocarcinogenesis was of interest from the therapeutic perception because this may aid in a coup, delay, or even prevent tumorigenesis [ 29 , 30 ]. Phytochemicals were shown to control HCC via interference with all phases of carcinogenesis, including initiation, promotion, and progression [ 31 , 32 ].…”

Potential Mechanisms of Yanghe Decoction in the Treatment of Soft Tissue Sarcoma and Arteriosclerosis Obliterans Based on Network Pharmacology

“…Interactions between cytokines and cytokine receptors can regulate the growth and differentiation of cells, regulate immune responses, participate in inflammatory responses, repair damaged tissues, and have regulatory effects on STS and ASO. [38][39][40][41] In addition, TNF signaling pathway, Th17 cell differentiation, and NOD-like receptor signaling pathway are all signal pathways related to immunity and inflammation, which can activate NF-κB, MAPK, and endoplasmic reticulum emergency pathway and promote the release of inflammatory factors such as IL-6 and mediate inflammatory response, which is closely related to tumors, inflammatory diseases, and autoimmune diseases. 42,43 Fig.…”