ArticleGenes & diseases2025
Galectin-3 in tumor-stromal cells enhances gemcitabine resistance in pancreatic adenocarcinoma by suppressing oxidative phosphorylation.
Article in Genes & diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Glycobiology-driven therapeutic targeting of glycan-binding proteins: mechanisms, diseases, and clinical translation.Signal transduction and targeted therapy · 2026Review
- Galectins at the crossroads of tumor immunity, metabolism, and metastasis: mechanisms, therapeutic resistance, and translational opportunities.Frontiers in immunology · 2026Review
- Overexpression of Nuclear Factor of Activated T-cells (NFAT) Transcription Factors Drives Chemoresistance and Poor Outcomes in Pancreatic Cancer.Annals of surgical oncology · 2025Article
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12 authors.
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Abstract
Galectin-3 (Gal-3) plays a multifaceted role in the development and progression of pancreatic adenocarcinoma (PAAD), which is associated with a poor prognosis. Its interaction with tumor microenvironment cells has been reported. However, the Gal-3-mediated tumor-stromal interaction and induced energy metabolism associated with drug resistance remain unknown. Our previous study has reported that Gal-3 secretion from tumor cells and inflammatory cytokine dependency are therapeutic targets. In this study, we revealed that the expression of Gal-3 was not only remarkably up-regulated in tumors but also significantly associated with the tumor-associated fibroblasts of PAAD patients. A coculture model of PAAD cells and pancreatic stellate cells revealed that Gal-3 mediated the Ca
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