To investigate the leukotriene (LT) D₄ (LTD₄) receptor (cysteinyl-LT₁ receptor [CysLT₁R]) expression in transitional cell carcinoma (TCC) of the bladder, as well as the effects of the CysLT₁R antagonist on cell proliferation in TCC cell lines. The metabolism of arachidonic acid by either cyclooxygenase or lipoxygenase is thought to play an important role in carcinogenesis. LTD₄ is a pro-inflammatory mediator derived from arachidonic acid through various enzymatic steps, and 5-lipoxygenase is an important factor in generating LTD₄.

CysLT₁R expression in TCC tissue and normal bladder tissue was examined. CysLT₁R expression was detected using immunohistochemistry. The effects of the CysLT₁R antagonist on TCC cell growth were examined by 3-(4,5-dimethylthiazol-2-thiazolyl)-2,5-diphenyltetrazolium bromide assay and reverse transcriptase-polymerase chain reaction. Flow cytometry was used to determine whether the CysLT₁R antagonist induced apoptosis.

Initially, only slight CysLT₁R expression was detected in normal bladder tissues and marked CysLT₁R expression was detected in the TCC tissues. CysLT₁R expression was greater in high-grade cancer than in low-grade cancer. Furthermore, CysLT₁R expression was also greater in advanced-stage cancer than in early-stage cancer. Finally, the CysLT₁R antagonist caused marked inhibition of TCC cells by inducing early apoptosis.

CysLT₁R was induced in TCC. The results suggest that the CysLT₁R antagonist might mediate potent antiproliferative effects on TCC cells. Thus, the target of the CysLT₁R is potentially a new therapy in the treatment of TCC.