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Molecular structure of
|Lecster ID:316|| Edit Entry |
| Common Nomenclature:||Galectin I|
|Class:||Proto S-lectin or galectin|
|Characterization Notes:||Human galectin I is a likely candidate as a novel target for gene therapy in the treatment of rheumatoid arthritis using endogenous biological mediators to induces apoptosis of activated T cells and immature thymocytes. See: Mem Inst Oswaldo Cruz 2000;95 Suppl 1:225-33 Up-regulation of galectin-1 in fibroblasts and galectin-3 in ductular complexes suggests a role of these lectins in tissue remodeling in chronic pancreatitis. See: Lab Invest 2000 Aug;80(8):1233-41|
|Biological Activity:||The expression pattern of galectin-1 pancreatic cancer tissues indicates that galectin-1 plays a role in the desmoplastic reaction that occurrs around pancreatic cancer cells. See:J Histochem Cytochem 2001 Apr;49(4):539-49 Studies reveal expression of galectin-1 in all human glioma types with no striking differences between astrocytic, oligodendroglial, and ependymal tumors. The level of galectin-1 expression correlated with the grade in the group of astrocytic tumors only. Furthermore, immunopositivity of high-grade astrocytic tumors from patients with short-term survival periods was stronger than that of tumors from patients with long-term survivals. In human glioblastoma xenografts, galectin-1 was preferentially expressed in the more invasive parts of these xenografts. In vitro experiments revealed that galectin-1 stimulates migration of U373 astrocytes. See: Glia 2001 Mar 1;33(3):241-55 Increased expression of galectin-1 in carcinoma-associated stroma predicts poor outcome in prostate carcinoma patients. The association between accumulation of galectin-1 in the stroma of the malignant tissue and aggressiveness of the tumour adds weight to the body of evidence that identifies a role for galectin-1 in the acquisition of the invasive phenotype. In addition to modulating cancer cell interactions with laminin, galectin-1 accumulated around the cancer cells may act as an immunological shield by inducing activated T-cell apoptosis. See: J Pathol 2001 Jan;193(1):80-7 The galectin-1 signal, however, strongly accumulates at the sites of cell-cell contacts predominantly on tumor cells, probably in concert with Thomsen-Friedenreich antigen. See: Cancer Res 2000 May 15;60(10):2584-8|
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