Galectins in Cancer, Fibrosis and Immune Modulation: Mechanisms, Therapeutic Strategies and Translational Advances
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".
Deadline for manuscript submissions: 31 October 2025 | Viewed by 877
Special Issue Editor
Special Issue Information
Dear Colleagues,
Galectins are key regulators of fibrosis, cancer progression, and immune modulation. These carbohydrate-binding proteins control immune suppression, extracellular matrix remodeling, epithelial–mesenchymal transition (EMT), and therapy resistance. Their influence extends beyond tumor biology, driving fibrotic diseases, such as hepatic, pulmonary, and cardiac fibrosis. For example, in cancer, Galectin-3 promotes tumor invasion and metastasis by facilitating integrin clustering and focal adhesion signaling. Galectin-9 contributes to immune evasion by inducing T-cell exhaustion, weakening antitumor responses. Galectin-1 plays a dual pathogenic role in cancer and fibrosis. In cancer, it induces T-cell apoptosis, impairing immune surveillance and reducing the effectiveness of checkpoint inhibitors. In fibrosis, it activates fibroblasts, leading to collagen deposition and tissue remodeling, which accelerates disease progression in the liver (hepatic fibrosis), lungs (pulmonary fibrosis), and heart (cardiac fibrosis).
This Special Issue aims to explore the following:
- The role of Galectins in treatment resistance and disease progression;
- The mechanisms by which Galectins drive immunosuppression, metastasis, and fibrosis;
- Therapeutic strategies targeting Galectins, including inhibitors, combination therapies, and immunomodulation.
By integrating findings across these fields, this Special Issue will advance our understanding of Galectin biology and its translational potential in cancer, fibrosis, and immune-related diseases.
Dr. Tsung-Chieh Shih
Guest Editor
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Keywords
- Galectin
- tumor microenvironment
- immunosuppression
- fibrosis
- epithelial–mesenchymal transition (EMT)
- cancer metastasis
- immune evasion
- therapy resistance
- myeloid-derived suppressor cells (MDSCs)
- tumor-associated macrophages (TAMs)
- extracellular matrix remodeling
- Galectin-targeted therapy
- combination immunotherapy
- fibroblast activation
- chronic inflammation
- tumor–stroma interactions
- novel inhibitors of Galectins
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