Disease relevance of Lgals7

• The present study was designed to investigate the role of galectin-7 in lymphoma [1].
• We also found that inhibition of galectin-7 in aggressive lymphoma cells correlated with a decreased invasion of tumor cells in target organs and a reduced expression of matrix metalloproteinase-9, a gene associated with a poor prognosis in non-Hodgkin's lymphoma [2].
• For example, up-regulation of galectin-7 is associated with rat mammary carcinomas and with progression to T-cell malignancy [2].

High impact information on Lgals7

• We found that stable transfection of lymphoma cells with a plasmid encoding antisense galectin-7 cDNA significantly inhibited the dissemination and invasion of lymphoma cells to peripheral organs, thereby increasing the survival of mice [2].
• We finally examined the expression of galectin-7 in 50 specimens of different mature B-cell neoplasms and found high galectin-7 expression levels in a significant proportion of mature B-cell neoplasms but not in normal B cells [2].
• A novel function for galectin-7: promoting tumorigenesis by up-regulating MMP-9 gene expression [1].
• We have recently identified galectin-7 as a new gene associated with the progression of T cell lymphoma toward a metastatic phenotype, suggesting a possible causal relationship [1].
• Gene expression analysis using cDNA microarrays revealed that healing corneas of gal3(-/-) mice contain markedly reduced levels of galectin-7 compared with those of gal3(+/+) mice [3].

Chemical compound and disease context of Lgals7

• We also showed that treatment of nonaggressive lymphoma cells with 5-aza-2'-deoxycytidine was sufficient to induce galectin-7 gene expression [4].

Biological context of Lgals7

• Moreover, transfection of an expression vector containing the galectin-7 gene in low metastatic lymphoma cells increased their metastatic behavior and confers these cells with the new ability to overcome the resistance of intercellular adhesion molecule-1-deficient mice to lymphoma dissemination [1].
• This suggested that galectin-7 expression might be induced at a particular stage in the embryonic development of stratified epithelia [5].

Anatomical context of Lgals7

• Galectin-7 expression in aggressive lymphoma cells was induced upon in vivo selection in several organs, including the thymus, the spleen and kidneys [4].
• Stratified epithelium from the lip to forestomach and anus intensely expressed galectin-7 with weak expressions of galectin-3 [6].
• Starting from E13.5, weak expression of galectin-7 was detected in bilayered ectoderm, and stronger expression was found in areas of embryonic epidermis where stratification was more advanced [5].
• In contrast, no expression of galectin-7 was found in epithelia derived from endoderm, such as lining of the intestine, kidney and lung [5].

Other interactions of Lgals7

• The extent of acceleration of re-epithelialization of wounds with both galectin-3 and galectin-7 was greater than that observed in most of the published studies using growth factors [3].
• Galectin-7 is a 14 KDa member of the galectin family that we have cloned from human, rat and mouse [5].

Analytical, diagnostic and therapeutic context of Lgals7

• In the present study we have investigated this hypothesis by in situ hybridization of galectin-7 mRNA in mouse embryos [5].

References