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CONCLUSION: Etodolac at clinical doses exhibited induced in vitro and in vivo anti-tumour effects and reversal effect of EMT in T24.

Although most cases of bladder cancer present as a superficial tumour, and are treated with transuretheral resection of the bladder tumour (TUR-BT), the recurrence rate after TUR-BT is high (30–85%) and approximately 10–30% of cases will progress to a muscle-invasive tumour that has a poorer prognosis (Pasin , 2008).Therefore, an effective strategy for preventing the progression of bladder cancer is clearly needed.Cyclooxygenase-2 (Cox-2) is overexpressed in high-grade invasive TCC, and the anti-tumour effect of Cox-2 inhibitors in invasive TCC of urinary bladder has been suggested in both pre-clinical and clinical studies (Okamoto , 2010).However, the mechanism of action for the anti-tumour effects of Cox-2 inhibitors is unclear.BACKGROUND: Although the anti-tumour effect of cyclooxygenase-2 (Cox-2) inhibitors in invasive bladder cancer has been confirmed, its mechanisms of action are unclear.

Recently, the concept of an epithelial-to-mesenchymal transition (EMT) promoting carcinoma progression has been suggested, and a key feature of the EMT is the downregulation of E-cadherin.In this study, we investigated the effect of Cox-2 inhibitors on reversal EMT and tumour growth inhibition in bladder cancer cells.METHODS: We used three Cox-2 inhibitors, etodolac, celecoxib and NS-398 and three human bladder cancer cell lines, T24, 5637 and KK47, in this study.T24 xenograft tumour mouse model was used in the in vivo study.RESULTS: Within the clinical drug concentrations, only etodolac showed the in vitro growth inhibition in T24 not in the other cell lines.Etodolac reduced SNAIL m RNA and vimentin cell surface expression, and induced E-cadherin m RNA and E-cadherin cell surface expression, in T24.