Galectin-3, a member of the
beta-galactoside-binding lectin family, is involved in a variety of
biological events including interactions with
galactose-containing
glycoconjugates, cell proliferation, differentiation and apoptosis.
Galectin-3 appears to intervene during
tumor progression and altered expression patterns have been reported in a variety of
malignancies. In our study, we have examined the expression of
galectin-3 in a population of 145 prostate
carcinoma samples using immunohistochemistry. We found that most of the non-tumoral prostatic glands exhibited moderate immunostaining for
galectin-3 localized in both nucleus and cytoplasm. In
prostatic cancer cells,
galectin-3 was usually not expressed or decreased compared with the normal glands. Interestingly, when
galectin-3 was detected in the
cancer cells, it was consistently excluded from the nucleus and only present in the cytoplasmic compartment. The latter observation was also made for
prostatic intraepithelial neoplasia (PIN) cells. Furthermore, we found that the levels of
galectin-3 expression in the
cancer cells were significantly associated with
prostate-specific antigen (PSA) relapse in univariate analysis (p = 0.044). Cytoplasmic expression of
galectin-3 in the
carcinoma cells was an independent predictor of
disease progression in multivariate analysis, after the pathological stage and the Gleason score. Our data demonstrate that
galectin-3 is generally down-regulated in human prostate
carcinoma cells, and consistently excluded from the nucleus. Interestingly, specific cytoplasmic expression of
galectin-3 in a subset of lesions is associated with
disease progression. These results suggest that
galectin-3 might play anti-
tumor activities when present in the nucleus, whereas it could favor
tumor progression when expressed in the cytoplasm. Further studies should determine the exact role and mechanisms by which
galectin-3 differentially affects cell behavior in the different locations where it is expressed.