Copy-number amplification drives IFI30 overexpression and coordinated immune activation, identifying a novel diagnostic and therapeutic target in gastric adenocarcinoma.

ABSTRACT: Interferon-γ-inducible protein 30 (IFI30, also known as lysosomal thiol reductase, GILT) plays a key role in antigen processing by reducing disulfide bonds. However, its biological significance in gastric cancer (GC) has not been systematically elucidated. This study integrated pan-cancer multi-omics data, including transcriptomics (TCGA-STAD, GEO), genomics (whole-exome somatic mutations, copy number alterations), immune profiling, single-cell RNA sequencing, and transcription factor prediction to comprehensively characterize the dysregulation of IFI30 in GC. Downstream pathway involvement was inferred through weighted gene co-expression network analysis (WGCNA), gene set enrichment analysis (GSEA), and phosphoproteomic correlation mapping. The immune microenvironment was analyzed using C

SUBMITTER: Liu Q 

PROVIDER: S-EPMC12917288 | biostudies-literature | 2026 Feb

REPOSITORIES: biostudies-literature