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Overexpression of galectin-7, a myoepithelial cell marker, enhances spontaneous metastasis of breast cancer cells


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Demers, Mélanie; Rose, April A.N.; Grosset, Andrée-Anne; Biron-Pain, Katherine; Gaboury, Louis; Siegel, Peter M. et St-Pierre, Yves ORCID logoORCID: https://orcid.org/0000-0002-1948-2041 (2010). Overexpression of galectin-7, a myoepithelial cell marker, enhances spontaneous metastasis of breast cancer cells American Journal of Pathology , vol. 176 , nº 6. pp. 3023-3031. DOI: 10.2353/ajpath.2010.090876.

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Galectins are members of a family of β-galactosides-binding proteins that have recently emerged as novel modulators in different aspects of cancer. The expression of galectins in tumors and/or the tissue surrounding them has been well documented. Since galectin-7 expression has been associated with epithelial tissues and varies significantly in various types of cancer, we have investigated for the first time its role in breast cancer. Using two preclinical mouse models, high levels of galectin-7 expression in breast cancer cells drastically increased their ability to metastasize to lungs and bones. Significant increases in the number of pulmonary metastases and osteolytic lesions were induced by overexpression of galectin-7 compared with control cells. In human tissues, galectin-7 was specifically found in myoepithelial cells of normal human breast tissue, but not in luminal cells. Its expression was severely altered in breast carcinoma, many samples showing greater than 70% of galectin-7 positive cells. High expression levels of galectin-7 were restricted to high-grade breast carcinomas, including HER2 overexpressing and basal-like groups. In HER2 overexpressing cases, galectin-7 expression was associated with lymph node axillary metastasis. Taken together, our results indicate that galectin-7 may represent a potential target for both specific detection and therapeutic inhibition of metastatic breast cancer.

Type de document: Article
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Centre: Centre INRS-Institut Armand Frappier
Date de dépôt: 29 juin 2024 21:45
Dernière modification: 29 juin 2024 21:45
URI: https://espace.inrs.ca/id/eprint/14579

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