AI Article Synopsis

  • - This study investigates the relationship between gastric cancer (GC) and infection, focusing on gene expression changes and regulatory networks involved in the progression from normal gastric tissue to atrophic gastritis (GA) and ultimately to GC.
  • - Researchers analyzed gene expression data and identified differentially expressed genes (DEGs) linked to digestion, cell proliferation, and immune regulation, creating lncRNA-TF-mRNA and ceRNA networks to understand the molecular mechanisms at play.
  • - Key findings highlight the importance of specific genes and regulatory networks, such as CDX2 and GATA5, which may provide insights into how infection-related changes contribute to the development of gastric diseases and could guide future research efforts.

Article Abstract

Background: () infection is the strongest risk factor for gastric cancer (GC). However, the mechanisms of -associated GC remain to be explored.

Methods: The gene expression profiling (GSE111762) data were downloaded from the GEO database. Differentially expressed genes (DEGs) between normal samples (NO) and -atrophic gastritis (GA) or -GA and -GC were identified by GEO2R. Gene Ontology and pathway enrichment analysis were performed using the DAVID database. lncRNA-TF-mRNA and ceRNA regulation networks were constructed using Cytoscape. The cross-networks were obtained by overlapping molecules of the above two networks. GSE27411 and GSE116312 datasets were employed for validation.

Results: DEGs between NO and -GA are linked to the activity of inward rectifying potassium channels, digestion, etc. DEGs between -GA and -GC were associated with digestion, positive regulation of cell proliferation, etc. According to the lncRNA-TF-mRNA network, 63 lncRNAs, 12 TFs, and 209 mRNAs were involved in -GA while 16 lncRNAs, 11 TFs, and 92 mRNAs were contained in the -GC network. In terms of the ceRNA network, 120 mRNAs, 18 miRNAs, and 27 lncRNAs were shown in -GA while 72 mRNAs, 8 miRNAs, and 1 lncRNA were included in the -GC network. In the cross-network, we found that immune regulation and differentiation regulation were important in the process of NO-GA. Neuroendocrine regulation was mainly related to the process of GA-GC. In the end, we verified that CDX2 plays an important role in the pathological process of NO to -GA. Comparing -GA with -GC, DEGs (FPR1, TFF2, GAST, SST, FUT9, and SHH), TF, and GATA5 were of great significance.

Conclusions: We identified the DEGs, and their lncRNA regulatory network of -associated diseases might provide insights into the mechanism between infection and GC. Furthermore, in-depth studies of the molecules might be useful to explore the multistep process of gastric diseases.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7686847PMC
http://dx.doi.org/10.1155/2020/3012193DOI Listing

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