Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P17931 (galectin-3)
 2,860 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Data from the literature now indicate that cancer cells can specifically interact with the unique extracellular matrix protein, elastin. The interaction is mediated by two elastin-binding proteins (EBP), S-gal/EBP (organized into the elasin receptor/elastonectin complex) and galectin-3, components of two laminin receptors. Studies revealed that the expression of both EBPs is closely associated to the invasive/metastatic potential of various cancer types. This is due to the fact that elastin-ligation of S-gal/EBP induces motogenic, as well as mitogenic signals and releases various elastases from cancer cells and the induction depends on the metastatic potential. Studies also demonstrated that certain cancer cells can synthesize elastin and express lysyl oxydase, providing explanation for frequent appearance of elastic tissue in tumors such as breast or gastric cancers. Clinico-pathological data suggest some correlation with tumor progression of the presence of the elastic tumor stroma. Since elastic tissue may be a significant reservoir of angiostatic molecule(s) this extracellular matrix protein can also have a role in tumor-induced angiogenesis. Soluble elastin as well as elastin peptides are potent inhibitors of the metastatic process in experimental tumor models. On the other hand, elastin peptides can also be used to design targeted therapies exploiting the unique physicochemical nature of this matrix protein. Altogether, these data suggest a significant role for tumor cell-elastin interactions in tumor progression.
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PMID:Role of elastin-matrix interactions in tumor progression. 1208 51

To investigate the relationship between osteofibrous dysplasia (OFD) and adamantinoma, we analyzed the expression of several proto-oncogene products and extracellular matrix proteins by immunohistochemistry and correlated our results with histological and ultrastructural findings. C-fos and c-jun, but not c-Met, were observed in OFD and in the fibrous and epithelial components of differentiated and classical adamantinomas. Staining for collagen IV, laminin and galectin-3, a laminin binding protein was seen in OFD and around cell nests in adamantinoma. E-, P-, and N-cadherin expression was found in all cases of classical adamantinoma, but not in differentiated adamantinoma or OFD. Osteonectin was detected in both the epithelial and fibrous components of adamantinomas, but osteopontin and osteocalcin were not seen in classical adamantinomas. The results show common expression of a number of oncoproteins and bone matrix proteins in adamantinoma and OFD, some of which are associated with mesenchymal-to-epithelial cell transformation. These findings would be in keeping with the hypothesis that OFD represents a precursor lesion of adamantinoma. Differential expression of a number of bone matrix protein in adamantinoma may also be of diagnostic use in distinguishing these 2 lesions immunohistochemically.
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PMID:Osteofibrous dysplasia and adamantinoma: correlation of proto-oncogene product and matrix protein expression. 1474 27

Atherosclerosis and renal disease are related conditions, sharing several risk factors. This includes hyperlipidaemia, which may result in enhanced lipoprotein accumulation and chemical modification, particularly oxidation, with formation of advanced lipoxidation endproducts (ALEs). We investigated whether increased lipid peroxidation plays a major role in the pathogenesis of lipid-induced renal disease, via receptor-mediated mechanisms involving the scavenger and advanced glycation endproduct (AGE) receptors. Mice knocked out for galectin-3 (Gal3(-/-)), an AGE receptor previously shown to protect from AGE-induced renal injury, and the corresponding wild-type (Gal3(+/+)) animals, were fed an atherogenic high-fat diet (HFD; 15% fat, 1.25% cholesterol and 0.5% sodium cholate); mice fed a normal-fat diet (NFD; 4% fat) served as controls. Gal3(+/+) mice fed a HFD developed glomerular disease, as indicated by proteinuria, mesangial expansion and glomerular hypertrophy and sclerosis. Glomerular injury was associated with increased glomerular matrix protein expression, ALE and oxidized LDL content, oxidative stress, AGE and scavenger receptor expression and macrophage infiltration, with only modest renal/glomerular fat accumulation and changes in lipid metabolism. Fibrotic and inflammatory changes, together with accumulation of ALEs, such as 4-hydroxy-2-nonenal adducts and N(epsilon)-carboxymethyllysine, oxidative stress and expression of the receptor of AGEs (RAGE), were significantly more marked in Gal3(-/-) animals, whereas fat deposition and abnormalities in lipid metabolism remained modest. Thus, lipid-induced renal damage is mainly dependent on lipid peroxidation with formation of carbonyl reactive species and ALEs, which accumulate within the kidney tissue, thus triggering receptor-mediated pro-inflammatory signalling pathways, as in atherogenesis. Moreover, galectin-3 exerts a significant role in the uptake and effective removal of modified lipoproteins, with diversion of these products from RAGE-dependent pro-inflammatory pathways associated with downregulation of RAGE expression.
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PMID:Advanced lipoxidation end-products mediate lipid-induced glomerular injury: role of receptor-mediated mechanisms. 1933 49