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Naito, Sei; Bilim, Vladimir; Kawazoe, Hisashi; Tomita, Yoshihiko
Cancer research (Chicago, Ill.), 04/2011, Volume: 71, Issue: 8_SupplementJournal Article
Abstract Introduction: Glycogen synthase kinase-3beta (GSK-3beta) is a serine/threonine kinase, as a positive regulator of several cancer cell survival and proliferation. We previously showed that nuclear accumulation of GSK-3beta indicates high grade, high stage, and poor survival in bladder urothelial cancer (UC). And inhibition of GSK-3beta suppresses UC cell proliferation and induces apoptosis via NF-kappaB down-stream genes viz. BCl-2 and XIAP (Clin Cancer Res 2010). Here we were to identify the interaction between cisplatin and GSK-3 inhibitor, AR-A014418 in UC. Experimental Procedures: We added cisplatin (0, 1, 3, 6 μg/ml) and AR-A014418 (0, 10, 20 μM) to medium in T24 and HT1376 human UC cells and assessed their viability by MTS assay. Furthermore, we intraperitoneally administrated PBS 5 time per week, 2.5 mg/kg body weight cisplatin once per week, 20 mg/kg body weight AR-A014418 5 time per week, or cisplatin and AR-A014418 into each 6 mice with subcutaneous xenografts of HT1376 for 3 weeks. Result: Treatment of cisplatin and AR-A014418 showed synergistic effect in cell lines. Cisplatin did not change expression level of GSK-3beta, and AR-A014418 suppressed XIAP for cell lines with cisplatin. The average tumor volume of the mice treated by cisplatin was equivalent to one by PBS within treatment period. However, the tumors treated by cisplatin grew bigger than ones by PBS after withdrawal of treatment. AR-A014418 inhibited the growth of tumor compared to PBS and cisplatin. And combine use of cisplatin and AR-A014418 prevented the tumor from re-growth by cisplatin after treatment. Body weight did not vary between mice by each treatment methods. Conclusion: Cisplatin and AR-A014418 synergistically suppressed UC cells viability. And AR-A014418 cancelled re-growth of low-dose cisplatin in xenograft model. Citation Format: {Authors}. {Abstract title} abstract. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2419. doi:10.1158/1538-7445.AM2011-2419
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