Fig 1.
Analysis of methylation in rats with GC.
(A) Images of gastric tissues from the control and GC groups. (B) HE staining of gastric tissues from the control and GC groups. (C) Pie charts show the genomic locations of the identified DMRs (promoter, 5′ UTR, exon, intron, 3′ UTR, intergenic). (D) Proportion of high/low methylation sites in each chromosome. GC, gastric cancer; HE, hematoxylin and eosin; DMRs, differentially methylated regions; UTR, untranslated region.
Fig 2.
(A) KEGG enrichment. (B) GO enrichment.
Fig 3.
Enrichment analysis of promoter-related genes in DMRs.
(A) KEGG enrichment. (B) GO enrichment.
Fig 4.
Transcriptome sequencing analysis of rats with GC.
(A) Heat map of DEGs. (B) Volcano plot of gene expression patterns. (C) Dot plot of GO enrichment. (D) Dot plot of KEGG enrichment. DEGs, differentially expressed genes; GO, Gene Ontology; KEGG, Kyoto Encyclopedia of Genes and Genomes.
Fig 5.
Screening of key genes and related analysis.
(A) Venn diagram of hypomethylated and highly expressed genes. (B) KEGG circle diagram analysis of key pathways and core genes related to hub genes. (C) mRNA expression level of DHX58 in GC and adjacent tissues from the TCGA database. (D) Spearman correlation analysis of DHX58 and inflammatory pathways. GC, GC-adjacent tissue; TCGA, TCGA. (E) Corresponding gene mutation profiles of the two groups with high and low DHX58 expression levels. DHX58, DExH-box helicase 58; TCGA, The Cancer Genome Atlas.
Fig 6.
Immune-related analysis of DHX58.
(A) TIMER analysis of the correlation between DHX58 expression and six types of immune cells. (B) EPIC analysis of the correlation between DHX58 expression and six types of immune cells. (C) Relationship between DHX58 expression and 10 immune checkpoint-related molecules. (D) TIDE score of DHX58 was used to analyze its ability to predict the efficacy of immunotherapy.
Fig 7.
Analysis of upstream transcription factors of DHX58.
(A) Preliminary screening of three transcription factors was conducted based on their binding sites within the CpG island region and the distribution frequency of these binding sites. (B) Western blotting was used to detect the expression levels of transcription factors in gastric tissues. (C) Knockdown efficiency of CEBPα in AGS cells was detected using PCR. (D) Western blotting was used to detect the expression of CEBPα and DHX58 in AGS cells. (E) Detection of the expression of CEBPα and DHX58 in rat gastric tissues. (F) Detection of DHX58 expression using MS-PCR. AGS, adenocarcinoma gastric stomach; CEBPα, CCAAT enhancer–binding protein α; MS-PCR, methylation-specific PCR.