Abstract
Despite recent advances in diagnosis and treatment, glioblastoma (GBM) represents the most common and aggressive brain tumor in the adult population, urging identification of new rational therapeutic targets. Galectins, a family of glycan-binding proteins, are highly expressed in the tumor microenvironment (TME) and delineate prognosis and clinical outcome in patients with GBM. These endogenous lectins play key roles in different hallmarks of cancer by modulating tumor cell proliferation, oncogenic signaling, migration, vascularization and immunity. Additionally, they have emerged as mediators of resistance to different anticancer treatments, including chemotherapy, radiotherapy, immunotherapy, and antiangiogenic therapy. Particularly in GBM, galectins control tumor cell transformation and proliferation, reprogram tumor cell migration and invasion, promote vascularization, modulate cell death pathways, and shape the tumor-immune landscape by targeting myeloid, natural killer (NK), and CD8+ T cell compartments. Here, we discuss the role of galectins, particularly galectin-1, -3, -8, and -9, as emerging glyco-checkpoints that control different mechanisms associated with GBM progression, and discuss possible therapeutic opportunities based on inhibition of galectin-driven circuits, either alone or in combination with other treatment modalities.
Highlights
Despite recent advances in diagnosis and treatment, glioblastoma (GBM) represents the most common and aggressive brain tumor in the adult population, urging identification of new rational therapeutic targets
These results indicated an extracellular role of galectin-3 on glioma migration
Given the involvement of galectin-3 in tumor angiogenesis [56], these results suggested a central role for this lectin during
Summary
Glycans were originally conceived as biomarkers of tumor malignancy and disease progression, recent evidence highlights their functional roles as key regulators of primary tumor growth and metastasis, introducing the concept of tumor “glyco-checkpoints”. This posed to play key roles in virtually all hallmarks of cancer and metastasis [42,43] This includes galectin-mediated programs that assist tumors in sustaining proliferation driven includes galectin-mediated programs that assist tumors in sustaining proliferation driven by oncogenic signaling circuits [44,45], evading growth suppressors [46,47], fostering inby oncogenic signaling circuits [44,45], evading growth suppressors [46,47], fostering flammation [48–50], activating invasion processes such as epithelial–mesenchymal transiinflammation [48–50], activating invasion processes such as epithelial–mesenchymal transition (EMT) and early dissemination [51–53], inducing angiogenesis [33,54–56], developing tion (EMT) and early dissemination [51–53], inducing angiogenesis [33,54–56], developing resistance to cell death [57,58], and avoiding immune destruction [59–63].
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