PD05.03. Galectin-3 is an Essential Player in Esophageal Adenocarcinoma Development and Progression : A Novel Prognostic Biomarker and Future Therapeutic Target

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ID: 326204
2026
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Abstract
Abstract Topic Esophageal Cancer: Barrett‘s Esophagus: High-Grade Dysplasia and Early Invasive Cancer Background Galectin-3, a β-galactoside-binding lectin, is known to enhance immunosuppression within the tumour microenvironment, promote metastasis and therapeutic resistance. Galectin-3 exhibits multiple pro-tumorigenic roles across different malignancies, however its role in esophageal adenocarcinoma (EAC) remains largely unknown. Targeting Gal-3 in combination with immune-checkpoints is a emerging strategy to improve clinical outcomes. Methods Galectin-3 and PD-L1 protein levels were assessed by Flow Cytometry and ELISA. Cellular viability, proliferation and cell cycle analysis was assessed using CCK8, BRDU and PI staining assays respectively. Representative esophageal normal, metaplastic, dysplastic and EAC cell lines were used to model disease progression. Tissue conditioned media (TCM) and tissue protein extracts were obtained from Barrett’s Esophagus (BE) patients, matched normal and EAC patient endoscopic biopsies. The Vienna grading system was implemented to group BE samples into non-dysplastic metaplasia, low grade dysplasia (LGD) and high grade dysplasia (HGD). Primary patient stromal cultures were isolated from fresh BE and EAC patient endoscopic samples. RNA analysis was carried out using illumina sequencing of BE progressor, non-progressor and EAC patients. In order to assess mechanistic underpinnings, STAT1 and STAT3 phosphorylation was assessed using western blot. Results Galectin-3 expression significantly increases across the normal-BE-EAC disease sequence in both nuclear and cytoplasmic compartments. Tissue protein extracts and TCM also show significant increases in Galectin-3 following the transition to HGD. This Galectin-3 upregulation in the premalignant setting likely reflects an important step in malignancy transition, evidenced by significantly higher Galectin-3 expression observed in BE patients who progressed to malignancy when compared to non-progressor controls. Inhibiting Galectin-3 significantly reduced EAC cell proliferation and viability without affecting BE, normal epithelia or primary tissue stroma. This inhibition also significantly reduced epithelial PD-L1 expression, while simultaneously increasing expression of the danger signal-calreticulin, transitioning cancer cells to a less immune-evasive and more immunogenic phenotype, again without affecting premalignant, normal epithelia or primary stroma. Finally, we have shown that Galectin-3 expression is significantly prognostic for EAC overall survival and recurrence-free survival with higher tumoral expression associated with poorer patient outcomes. Conclusion These results clearly implicate Galectin-3 as an essential player in the transition from premalignant BE to EAC, which was previously unknown. Galectin-3 has prognostic value in both outlining high risk BE-EAC progressors and EAC patient outcomes, with potential utility in surveillance. Excitingly, Galectin-3 inhibition could offer a selective treatment approach, either alone or in combination with immunotherapy for EAC. Reducing cancer cell survival and enhancing anti-tumour immunity, without affecting non-malignant tissue.
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Authors Sam Cahill, Enya Scanlon, Lorraine Smith, Cian Gargan, Erin Kindelon, Aideen Ryan, Richard Turkington, Joanne Lysaght
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Journal diseases of the esophagus : official journal of the international society for diseases of the esophagus
Year 2026
DOI
10.1093/dote/doag077.106
URL
https://doi.org/10.1093/dote/doag077.106
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