Induction of differentiation and apoptosis in the prostate cancer cell line LNCaP by sodium butyrate and galectin-1

Galectin-1 has been implicated in the process of vertebrate developmental r egulation. Sodium butyrate is an established differentiation-inducing agent and has been shown to increase galectin-1 expression in colon carcinoma ce lls. We studied the roles of butyrate and galectin-1 in the induction of di fferentiation and apoptosis in the prostate cancer cell line LNCaP. Treatme nt of LNCaP cells with butyrate resulted in induction of galectin-1 express ion in a time- and dose-dependent manner. Treatment with butyrate also resu lted in inhibition of proliferation, morphologic changes consistent with a differentiated phenotype, and induction of apoptosis. Prostate specific ant igen expression was transiently reduced. To determine which of these effect s might be secondary to the induction of galectin-1, LNCaP cells were trans fected with a galectin-1 expression vector. The transfected cells displayed growth inhibition and an increased rate of apoptosis. PSA expression was n ot affected. We conclude that galectin-1 may be responsible for many of the phenotypic changes resulting from butyrate treatment and may function down stream in the pathway of butyrate-induced differentiation. We also found PS A to be somewhat inconsistent as an indicator of differentiation of LNCaP c ells, likely due to other factors influencing its expression.