Glycobiology Advance Access published online on October 10, 2008
Glycobiology, doi:10.1093/glycob/cwn105
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Genetic assessment of the importance of galectin-3 in cancer initiation, progression and dissemination in mice
1 Institut Jacques Monod, UMR CNRS 7592, Univ. P6 and P7, 2 Place Jussieu, 75251 Paris Cedex 5, France
2 Angiogenesis Laboratory, Department of Pathology, School for Oncology and Developmental Biology, University of Maastricht, The Netherlands
3 Department of Cell Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA
4 Assistance Publique-Hôpitaux de Paris (AP-HP) Hôpital R. Debré, Service de Chirurgie Pédiatrique, Paris, France
# Author for correspondence: Françoise Poirier, Tour 43, 2 Place Jussieu, 75251 Paris, France, e-mail: poirier{at}ijm.jussieu.fr, Tel: 33 1 44 27 40 35, Fax: 33 1 44 27 52 65
Received on May 2, 2008; accepted on October 1, 2008
The galectin family of β-galactoside binding lectins is involved in normal and pathological processes. Altered expression of galectin-3 has been described in many cancers, and studies of cancer cell lines have implicated this lectin in various aspects of the tumorigenic cascade. The goal of this report was to directly assess the importance of galectin-3 in tumor biology by introducing the galectin-3 null mutation (galectin-3–/-) into mouse lines genetically programmed to develop cancers. We used two mouse models of human intestinal cancer, the ApcMin and Apc1638N lines, to study tumor initiation and tumor progression. We also crossed the galectin-3–/- mice with PyMT transgenic animals, a model in which primary mammary gland tumors give rise to lung metastases at high frequency. Unexpectedly, we show that the absence of galectin-3 does not affect the evolution of the disease in any of these three situations.
Key words: Apc mutations / galectin-3 knock out mice / metastasis / PyMT transgenics / tumor progression
* both authors equally contributed to the work