Comparing the Immunoexpression of FUT3 and FUT6 between Prostatic Adenocarcinoma and Benign Prostatic Hyperplasia

Abstract

Prostatic Adenocarcinoma (PA) and Benign Prostatic Hyperplasia (BPH) have their etiology not fully understood mainly in glycidic aspects. Glycan changes are associated with cell alterations where glycosylation is carried out by glycosyltransferases, such as fucosyltransferases (FUTs). These enzymes catalyze the insertion of L-fucose residues in a variety of glycan structures often in the final stage of glycosylation. The present study aimed to investigate the expression of FUT3 and FUT6 in PA and BPH as well as to correlate immunostaining of these transferases with PA clinic-histopathologic data. The FUT3 and FUT6 expressions were evaluated by immunohistochemistry in formalin-fixed, paraffin-embedded biopsies of PA (n=40) and BPH (n=40). FUT3 and FUT6 showed a high expression in both prostatic diseases, especially FUT6. FUT6 was more immunoexpressed in PA cases than the FUT3 (p<0.0001) as well as in BPH cases but in a not significant way (p=0.0661). Besides, FUT3 was more expressed in BHP lesion than in PA cases (p<0.0001). Our study presented a new data about FUT3 and FUT6 expression in PA and BPH, revealing high FUT6 expression in both lesions and FUT3 overexpression in BHP in relation to PA, proposing that this enzyme could be a promising biomarker for benign prostate alterations.

Sec1 Regulates Intestinal Mucosal Immunity in A Mouse Model of Inflammatory Bowel Disease

“…FUT2 is known to be involved in the pathogenesis of many diseases, including colorectal cancer, pancreatic cancer (21), prostate cancer (22), peptic ulcer (23), atrophic gastritis (24), diabetes (25), and coronary heart disease (26). Association of FUT2 with IBD in humans has been studied by several other groups, using Fut2 −/− mice as the proxy (10).…”