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Cell and Tumor Biology |
1 INRS-Institut Armand-Frappier, University of Québec, Laval, Québec, Canada and 2 Centre National de la Recherche Scientifique, UPR 2169, "Instabilité Génétique et Cancer", Institut Gustave-Roussy, Villejuif, France
Requests for reprints: Yves St-Pierre, INRS-Institut Armand-Frappier, University of Quebec, 531 Boulevard Des Prairies, Laval, Quebec, Canada, H7V 1B7. Phone: 450-686-5354; Fax: 450-686-5501; E-mail: yves.st-pierre{at}inrs-iaf.uquebec.ca.
Metastasis is a multistep process by which cancer cells, after acquiring several capabilities, spread to distinct sites in the body. It is the major cause of death in individuals suffering from cancer. 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. The present study was designed to investigate the role of galectin-7 in lymphoma. We found that the development of thymic lymphoma was accelerated when induced by lymphoma cells overexpressing galectin-7. 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-1deficient mice to lymphoma dissemination. Finally, we provide data suggesting that galectin-7 modulates the aggressive behavior of lymphoma cells by controlling the expression of metastatic genes, such as MMP-9. This hypothesis is based on the following evidence: (a) galectin-7 transfectants have higher levels of MMP-9 expression, (b) addition of ß-lactose completely inhibits expression of MMP-9 by galectin-7 transfectants, and (c) recombinant forms of galectin-7 induces the expression of MMP-9 in both mouse and human lymphoma cells. Our results have uncovered the existence of a previously undescribed activity, the promotion of cancer cell malignancy, to galectin-7.
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