Identification of hub genes in gastric cancer by integrated bioinformatics analysis

Abstract

Background: Gastric cancer (GC) is one of the most common cancer worldwide. With the high rates of metastasis and recurrence, its overall survival remains poor at the present time. Hence, seeking new potential therapeutic targets of GC is important and urgent.Methods: We retrieved the gene expression profiles and clinical data from The Cancer Genome Atlas (TCGA) datasets. After screening differentially expressed genes (DEGs), we carried out the survival analysis for overall survival to pick out robust DEGs. To explore the role of these robust DEGs, we conducted Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analyses.Subsequently, protein interactions network was constructed utilizing the Search Tool for the Retrieval of Interacting Genes (STRING) database. We then presented the module analysis and filtered out hub genes by the Cytoscape software. Finally, Kaplan-Meier analysis was utilized to demonstrate the prognostic role of these hub genes.Results: According to the gene expression profiles of TCGA and the survival analysis, 238 robust DEGs were filtered out, consisting of 140 up-regulated and 98 down-regulated genes. The up-regulated DEGs were mainly enriched in systemic lupus erythematosus, cytokine activity, and alcoholism, while downregulated DEGs were mainly enriched in steroid hormone receptor activity, immune response, and metabolism. Through the construction of the protein-protein interaction (PPI) network, eight hub genes were finally screened out, including CCR8, HIST1H3B, HIST1H2AH, HIST1H2AJ, NPY, HIST2H2BF, GNG7, and CCL25.Conclusions: Our study picked out eight hub genes, which might be potential prognostic biomarkers for GC and even be treatment targets for clinical implication in the future.

Hub genes and pathways in gastric cancer: A comparison between studies that used normal tissues adjacent to the tumour and studies that used healthy tissues as calibrator

“…Also, the GO enrichment analysis was shown that DEGs in the N and NAT lists were enriched in some similar terms, such as extracellular matrix organisation, retinol metabolism, and metabolism of xenobiotics by cytochrome P450. These GO terms were also have been reported for DEGs of GC in the previous reports [20][21][22]. However, some KEGG and GO terms were different for the N and NAT lists.…”

“…Also, the top protein module of the PPI network of the N and NAT list were enriched in the same KEGG terms. These KEGG terms were also reported for GC by Lu et al [20], who analysed seven microarray datasets with NAT tissues as calibrators, Sun et al [21], who analysed the TCGA database, Li et al [22], who analysed two microarray datasets, Zhang et al [23], who analysed three microarray datasets, and Zhang et al [24], who analysed one microarray dataset and TCGA database. Also, the GO enrichment analysis was shown that DEGs in the N and NAT lists were enriched in some similar terms, such as extracellular matrix organisation, retinol metabolism, and metabolism of xenobiotics by cytochrome P450.…”

“…[ 20 ], who analysed seven microarray datasets with NAT tissues as calibrators, Sun et al. [ 21 ], who analysed the TCGA database, Li et al. [ 22 ], who analysed two microarray datasets, Zhang et al.…”

CLCA1 is Poorly Expressed in Stomach Adenocarcinoma and Correlates with Immune Infiltration

“…Deviations in this pathway significantly contribute to tumor invasion and metastasis (Krabbe et al, 2016). Furthermore, there is an association between the occurrence of stomach cancer and systemic lupus erythematosus (SLE) (Sun et al, 2021). In support of this connection, Clarke et al (2021) conducted a meta-analysis and found that individuals with SLE had a significantly higher likelihood of developing gastric cancer.…”

Iroquois Family Genes in Gastric Carcinogenesis: A Comprehensive Review

“…They found that IRX4 was downregulated in the mouse stomach after irradiation with 6 or 12 Gy X-rays, and they also observed that radiation resulted in atrophy of the gastric mucosa and abnormal morphology of chief and parietal cells. Using the TCGA database, Sun and colleagues [ 110 ] identified that IRX4 expression was downregulated in GC patients and associated with their survival outcomes.…”