BACKGROUND: Galectin-3 is a beta-galactoside-binding vertebrate lectin. In @entity1 @entity263 , galectin-3 expression has been shown to decrease with progression of disease. In the present study, we further investigated the role of galectin-3 in this malignancy by examining the phenotype of galectin-3-transfected @entity263 cells. METHODS: Stably transfected galectin-3-expressing cell lines were developed from the @entity263 cell line LNCaP, which does not constitutively express this molecule. Transfected cells lines were analyzed for alterations in morphology and growth rates, and for ability to form @entity5 in @entity19 . RESULTS: Morphologically, when compared to the parental LNCaP cells, the galectin-3 transfectants had broader, flatter cell bodies, shorter and less finely branched dendritic processes, and large nuclei with pronounced and often multiple nucleoli. The galectin-3 lines were found to proliferate at a slower rate in vitro than either the vector control-transfected lines or parental LNCaP. When injected subcutaneously in @entity19 , four of six galectin-3 lines formed @entity5 at a slower rate than control lines. Twenty-four @entity5 that formed from the transfected cell lines were examined by immunohistochemistry for galectin-3 expression. Only one @entity5 was found to express galectin-3, suggesting that the transfected cells which formed @entity5 were those which successfully down-regulated galectin-3 expression. CONCLUSIONS: In contrast to an apparent stimulatory role in some @entity5 types, galectin-3 is an inhibitory molecule for @entity263 .

Effects of galectin-3 expression on growth and tumorigenicity of the XXXX cell line LNCaP.

@entity1 :: ('9606', 'Species') :: ['human'] @entity19 :: ('10090', 'Species') :: ['nude mice'] @entity263 :: ('MESH:D011471', 'Disease') :: ['prostate cancer'] @entity5 :: ('MESH:D009369', 'Disease') :: ['tumor', 'tumors']
@entity263 :: (MESH:D011471,Disease) :: ['prostate cancer']
