Discover oncology · 2026
Galectin 3 expression in gastrointestinal tumors identified through comprehensive bioinformatic mapping.
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Chiriva-Internati Maurizio, Grizzi Fabio, Hegazi Mohamed A A A, Figueroa Jose A, Bresalier Robert S
Аннотация
BACKGROUND: Gastrointestinal (GI) cancers are a major global health burden with high incidences 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.
CONCLUSIONS: These findings suggest LGALS3 as a promising diagnostic and prognostic biomarker, and a potential therapeutic target to enhance immune responses in GI cancers.
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.
CONCLUSIONS: These findings suggest LGALS3 as a promising diagnostic and prognostic biomarker, and a potential therapeutic target to enhance immune responses in GI cancers.