Fig 2: Functional analysis of C5aR1 in gastric cancer. (A) Heatmap of differentially expressed DEGs between the high and low C5aR1 expression groups. (B) and (C) C5aR1-related KEGG enrichment analysis (D)–(F) C5aR1-related GO function annotation. DEG: Differentially expressed genes; C5aR1: C5a receptor 1; GO: Gene Ontology; KEGG: Kyoto Encyclopedia of Genes and Genomes.

Fig 3: Correlation between C5aR1 expression and 22 common immune checkpoint-related genes in gastric cancer. (A) Differential expression of 22 immune checkpoint-related genes in the high and low C5aR1 expression groups; (B) Correlation between C5aR1 and 22 immune checkpoint-related genes in gastric cancer; (C)–(F) Correlation between the expression of C5aR1 and LAG3, CD274, CTLA4, and PDCD1 was analyzed using TIMER. C5aR1: C5a receptor 1; TIMER: Tumor Immune Estimation Resource.

Fig 4: Gene set enrichment analysis (GSEA). (A) GSEA of the top 10 upregulated pathways associated with C5aR1 in gastric cancer; (B) Natural killer cell-mediated cytotoxicity; (C) Cytokine receptor interaction; (D) Chemokine signaling pathway; (E) Toll-like receptor signaling pathway. C5aR1: C5a receptor 1.

Fig 5: The expression of C5aR1 in gastric cancer tissues and adjacent normal tissues. (A) C5aR1 expression was upregulated in GC tissues in the TCGA cohort. (B)–(D) C5aR1 expression was enhanced in GC tissues in the (B) GSE13911, (C) GSE29272, and (D) GSE54129 datasets; (E) C5aR1 was overexpressed in GC tissues in contrast to the paraneoplastic tissues in the TCGA cohort; (F) qRT-PCR depicted that expression of C5aR1 was significantly enhanced in GC tissues compared to normal tissues; (G) Immunohistochemical assessment showed that expression of C5aR1 was significantly enhanced in GC tissues compared to adjacent normal tissues (*P < 0.05; **P < 0.01; ***P < 0.001). C5aR1: C5a receptor 1; GC: Gastric cancer; TCGA: The Cancer Genome Atlas; qRT-PCR: Quantitative real-time polymerase chain reaction.