Galectin 3 Expression in Gastrointestinal Tumors Identified Through Comprehensive Bioinformatic Mapping 2334800

Abstract Introduction Abstract Background Gastrointestinal (GI) cancers are a major global health burden with high incidence and mortality. Despite advances in detection and treatment, prognosis for advanced disease remains poor, underscoring the need for new biomarkers and therapies. Galectin-3 (GAL-3), encoded by LGALS3, is a multifunctional β-galactoside-binding protein involved in adhesion, migration, apoptosis, angiogenesis, and immune regulation, making it an important modulator of tumor biology. Methods This study used in silico bioinformatic analyses to examine LGALS3 expression and its relationship with immune infiltration across seven GI cancers: cholangiocarcinoma (CHOL), colon adenocarcinoma (COAD), esophageal adenocarcinoma (ESCA), liver hepatocellular carcinoma (LIHC), pancreatic adenocarcinoma (PAAD), rectal adenocarcinoma (READ), and stomach adenocarcinoma (STAD) Results LGALS3 was significantly upregulated in CHOL, ESCA, and LIHC, with higher but non-significant expression in PAAD and STAD, while downregulated in COAD and READ. Elevated GAL-3 expression correlated with poorer survival, particularly in LIHC and PAAD. Immune infiltration analysis indicated a role in fostering an immunosuppressive tumor microenvironment. Protein—protein interaction analysis identified MAPK3 and PTEN as key partners, while Gene Ontology enrichment highlighted functions in T-cell activation and motility regulation. Conclusion These findings suggest LGALS3 as a promising diagnostic and prognostic biomarker, and a potential therapeutic target to enhance immune responses in GI cancers. Funding Source No Topic Categories Computational and Systems Immunology (COMP)