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This study aims to analyze LGALS3 expression and its implications in various gastrointestinal cancers using bioinformatic techniques.

June 12, 2026Discover Oncology0 citationsOpen Access

Galectin 3 expression in gastrointestinal tumors identified through comprehensive bioinformatic mapping

MCMaurizio Chiriva‐InternatiThe University of Texas MD Anderson Cancer Center FGFabio GrizziHumanitas University MHMohamed A.A.A. HegaziIRCCS Humanitas Research Hospital

Key Points

This study aims to analyze LGALS3 expression and its implications in various gastrointestinal cancers using bioinformatic techniques.
Conducted in silico bioinformatic analyses of LGALS3 expression across seven gastrointestinal cancers.
Examined the correlation between GAL-3 expression and immune infiltration, survival outcomes, and protein interactions.
Performed Gene Ontology enrichment to assess functions related to immune activation and tumor microenvironment.
LGALS3 expression was significantly upregulated in cholangiocarcinoma, esophageal adenocarcinoma, and liver cancer.
Elevated GAL-3 expression correlated with poorer survival, especially in liver and pancreatic cancers.
Identified MAPK3 and PTEN as key partners in protein interactions, highlighting LGALS3's role in immune modulation.

Abstract

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.

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