Down-regulation of galectin-3 suppresses tumorigenicity of human breast carcinoma cells

Galectin-3 is an endogenous P-galactoside-binding protein with specificity for type I and II ABH blood group epitopes and poly-N-acetyllactosamine gly can-containing cell surface glycoproteins and is the major nonintegrin cell ular 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 bre ast carcinoma MDA-MB-435 cells. Inhibition of galectin-3 expression led to reversion of the transformed phenotype as determined hy altered morphology, loss of serum-independent growth, acquisition of growth inhibition propert ies by cell contact, and abrogation of anchorage-independent growth. The bl ockage of galectin-3 expression led to a significant suppression of tumor g rowth in nude mice. These results provide direct evidence that galectin-3 e xpression is necessary for the maintenance of the transformed and tumorigen ic phenotype of MDA-MB-435 breast carcinoma cells.