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Clinical Cancer Research Vol. 7, 661-668, March 2001
© 2001 American Association for Cancer Research

Experimental Therapeutics, Preclinical Pharmacology

Down-Regulation of Galectin-3 Suppresses Tumorigenicity of Human Breast Carcinoma Cells1

Yuichiro Honjo2, Pratima Nangia-Makker, Hidenori Inohara and Avraham Raz3

Tumor Progression and Metastasis, Karmanos Cancer Institute and Department of Pathology, Wayne State University, School of Medicine, Detroit, Michigan 48201 [Y. H., P. N-M., A. R.], and Department of Otolaryngology and Sensory Organ Surgery, Osaka University Graduate School of Medicine, Osaka 565-0871, Japan [H. I.]

Galectin-3 is an endogenous ß-galactoside-binding protein with specificity for type I and II ABH blood group epitopes and poly-N-acetyllactosamine glycan-containing cell surface glycoproteins and is the major nonintegrin cellular laminin-binding protein. Galectin-3 is expressed at an elevated level in a wide range of neoplasms, and expression was shown to be associated in some tumor cell systems with metastases. Here we determined the functional consequence of blocking galectin-3 expression in highly malignant human breast carcinoma MDA-MB-435 cells. Inhibition of galectin-3 expression led to reversion of the transformed phenotype as determined by altered morphology, loss of serum-independent growth, acquisition of growth inhibition properties by cell contact, and abrogation of anchorage-independent growth. The blockage of galectin-3 expression led to a significant suppression of tumor growth in nude mice. These results provide direct evidence that galectin-3 expression is necessary for the maintenance of the transformed and tumorigenic phenotype of MDA-MB-435 breast carcinoma cells.




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Copyright © 2001 by the American Association for Cancer Research.