Etodolac, a Selective Cyclooxygenase-2 Inhibitor, Induces Upregulation of E-Cadherin and Has Antitumor Effect on Human Bladder Cancer Cells In Vitro and In Vivo - 23/08/11
, Toshinori Bito c, Katsumi Shigemura b, Katsuyuki Hamada d, Akinobu Gotoh e, Masato Fujisawa b, Masato Kawabata a
Reprint requests: Toshiro Shirakawa, M.D., Ph.D., International Center for Medical Research and Treatment, Kobe University School of Medicine, 7-5-1, Kusunoki-cho, Chuo-ku, Kobe 650-0017 Japan.Résumé |
Objectives |
Cyclooxygenase-2 (COX-2) is highly expressed in several human cancers, including bladder cancer. Thus, a selective COX-2 inhibitor could be useful as an antitumor agent for a range of cancers. In the present study, we investigated the antitumor effect and E-cadherin induction of etodolac, a highly selective COX-2 inhibitor, on human bladder cancer cells in vitro and in vivo.
Methods |
We examined the cytotoxicity of etodolac against three human bladder cancer cell lines, T24, 5637, and KK47, and performed quantitative reverse transcriptase-polymerase chain reaction to measure the mRNA expression of COX-2, and E-cadherin.
Results |
Etodolac showed significant cytotoxicity only to T24 cells, which expressed the greatest level of COX-2 mRNA and the lowest level of E-cadherin mRNA among the three cell lines. Etodolac also increased the E-cadherin mRNA expression in T24 cells in vitro. We also found that etodolac suppressed tumor growth and induced E-cadherin expression and cell apoptosis in a T24 tumor xenograft mouse model.
Conclusions |
Etodolac exhibited antitumor activity and induced E-cadherin expression in bladder cancer cells and might be useful for the clinical treatment and prevention of bladder cancer, especially in poorly differentiated bladder cancer with high COX-2 and low E-cadherin expression.
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Vol 71 - N° 1
P. 156-160 - janvier 2008 Retour au numéro
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