ABSTRACT
BACKGROUND: Galectin-3 is a carbohydrate-binding protein whose level of expression has been shown to be correlated with metastatic potential in a number of different tumor types. The purpose of this investigation was to examine galectin-3 expression in several tumorigenic and nontumorigenic prostate cell lines and prostate tissue samples. METHODS: The expression of galectin-3 in cell lines and tissue samples was evaluated by tissue immunohistochemistry and Western blot analysis. RESULTS: Human cell lines PC-3M, PC-3, DU-145, PrEC-1, and MCF10A demonstrated the presence of galectin-3. Galectin-3 was not detected in TSU-pr1 and LNCaP by Western blot analysis. We furthered our studies by examining a series of human prostate tissue samples for expression of galectin-3. Overall, approximately 60-70% of the normal tissue examined demonstrated heterogenous expression of galectin-3. In stage II tumors, however, there was a dramatic decrease in galectin-3 expression in both PIN and tumor sections, with only 10.5% (2/19) of these samples expressing this protein. Stage III tumors also demonstrated a decreased expression of galectin-3, although this downregulation was not as dramatic, with 35% of PIN samples and 52% of tumor tissue expressing galectin-3 (P < 0.01). CONCLUSIONS: These data demonstrate that galectin-3 is downregulated in prostate cancer. The altered downregulation pattern of galectin-3 observed between tumor stages suggests different roles for galectin-3 in the progression of prostate cancer.
Subject(s)
Antigens, Differentiation/biosynthesis , Gene Expression Regulation, Neoplastic , Prostate/pathology , Prostatic Neoplasms/pathology , Antigens, Differentiation/analysis , Antigens, Differentiation/genetics , Blotting, Western , Cell Line , Galectin 3 , Humans , Immunohistochemistry , Male , Prostate/cytology , Prostatic Neoplasms/chemistry , Prostatic Neoplasms/genetics , Tumor Cells, CulturedABSTRACT
BACKGROUND: The etiology of prostate cancer is currently a mystery. Several epidemiological studies suggest a link between dietary fat and prostate cancer. In vitro and in vivo studies support this evidence. Using the Dunning model of rat prostate cancer we hypothesized that a high-fat diet (20%) would increase the growth of the R3327-H tumor. MATERIALS AND METHODS: R3327-H tumors were implanted subcutaneously into male Copenhagen rats which were fed diets with 5 or 20% total fat. Tumors were allowed to grow for 16 weeks; they were then excised and weighed. The initial and final weights of the rats were also recorded. RESULTS: Statistical analysis revealed the level of dietary fat was a positive predictor of weight gain (p < 0.01). No effect on tumor growth was seen when compared to dietary fat, fiber type, or the interaction of fat and fiber. DISCUSSION: Growth of the R3327-H tumor, when implanted subcutaneously, is not affected by the level of dietary fat.
