To better understand whether overexpression of FUT8 might be responsible for castration-resistant phenotype in prostate cancer cells, we ectopically overexpressed FUT8 in LAPC4 cells and found that overexpression of FUT8 in LAPC4 cells suppressed the production of PSA, while knocking down the endogenous FUT8 with shRNA in LAPC4 cells significantly enhanced PSA production (Fig. 3a). This evidence concerns the gene KLK3 and prostate cancer.