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Blood, 15 June 2006, Vol. 107, No. 12, pp. 4880-4887. Prepublished online as a Blood First Edition Paper on February 23, 2006; DOI 10.1182/blood-2005-08-3423. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-08-3423v1 107/12/4880    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Che, X.-F. Articles by Akiyama, S.-i. Search for Related Content PubMed PubMed Citation Articles by Che, X.-F. Articles by Akiyama, S.-i. Related Collections Neoplasia Apoptosis Gene Expression Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Overexpression of survivin in primary ATL cells and sodium arsenite induces apoptosis by down-regulating survivin expression in ATL cell lines Xiao-Fang Che, Chun-Lei Zheng, Satsuki Owatari, Masato Mutoh, Takenari Gotanda, Hei-Cheul Jeung, Tatsuhiko Furukawa, Ryuji Ikeda, Masatatsu Yamamoto, Misako Haraguchi, Naomichi Arima, and Shin-ichi Akiyama From the Department of Molecular Oncology, Graduate School of Medical & Dental Sciences, and Department of Hematology and Immunology, Kagoshima University Hospital, Center for Chronic Viral Diseases, Division of Host Response, Kagoshima University, Sakuragaoka, Japan; and Pharmaceutical Research Laboratories, Toray Industries, Kamakura-city, Kanagawa, Japan. Patients with acute- or lymphoma-type adult T-cell leukemia (ATL) have a poor outcome because of the intrinsic drug resistance to chemotherapy. Protection from apoptosis is a common feature involved in multidrug-resistance of ATL. IAP (inhibitor of apoptosis) family proteins inhibit apoptosis induced by a variety of stimuli. In this study, we investigated the expression of IAP family members (survivin, cIAP1, cIAP2, and XIAP) in the primary leukemic cells from patients with ATL. We found that survivin was overexpressed in ATL, especially in acute-type ATL. Sodium arsenite was shown to down-regulate the expression of survivin at both the protein and RNA levels in a time- and dose-dependent manner, thus inhibiting cell growth, inducing apoptosis, and enhancing the caspase-3 activity in ATL cells. Nuclear factor-B (NF-B) enhances the transcriptional activity of survivin. Sodium arsenite suppressed the constitutive NF-B activation by preventing the IB- degradation and the nuclear translocation of NF-B. These findings suggest that survivin is an important antiapoptotic molecule that confers drug resistance on ATL cells. Sodium arsenite was shown to down-regulate the expression of survivin through the NF-B pathway, thus inhibiting cell growth and promoting apoptosis of ATL cells. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: E. Weisberg, A. L. Kung, R. D. Wright, D. Moreno, L. Catley, A. Ray, L. Zawel, M. Tran, J. Cools, G. Gilliland, et al. Potentiation of antileukemic therapies by Smac mimetic, LBW242: effects on mutant FLT3-expressing cells Mol. Cancer Ther., July 1, 2007; 6(7): 1951 - 1961. [Abstract] [Full Text] [PDF]

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