Galectins at the crossroads of tumor immunity, metabolism, and metastasis: mechanisms, therapeutic resistance, and translational opportunities - Report - MDSpire
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Galectins at the crossroads of tumor immunity, metabolism, and metastasis: mechanisms, therapeutic resistance, and translational opportunities
Clinical Report: Galectins in Tumor Immunity and Metabolic Changes
Overview
Galectins play crucial roles in tumor immunity, metabolic changes, and metastatic processes. This review synthesizes evidence on major galectin family members, particularly Gal-1, Gal-3, Gal-4, Gal-7, Gal-9, and Gal-13, and their mechanisms in driving tumor progression and therapeutic resistance.
Background
Cancer remains a leading cause of mortality, with immune evasion and therapeutic resistance posing significant challenges. Galectins, a family of β-galactoside-binding lectins, are emerging as key regulators in the tumor microenvironment. Understanding their roles could inform new therapeutic strategies.
Data Highlights
No numerical data or trial data presented in the article.
Key Findings
Galectins induce T-cell dysfunction via TIM-3 and PD-1 signaling.
They reprogram macrophages and myeloid-derived suppressor cells through PI3K/AKT, JAK/STAT, and NF-κB pathways.
Galectins modulate innate immune effectors like NK cells and dendritic cells in a context-dependent manner.
They influence tumor metabolism, affecting glycolysis and lipid metabolism.
Galectins are implicated in resistance to chemotherapy, targeted therapy, and immune checkpoint blockade.
Emerging galectin-directed strategies include small-molecule inhibitors and combination therapies.
Clinical Implications
Galectins are implicated in immune regulation and metabolic adaptation. Understanding their mechanisms may aid in developing strategies to overcome therapeutic resistance in cancer treatment.
Conclusion
Galectins are integral to tumor progression and therapeutic resistance.
