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Induction of apoptosis by HBI-8000 in adult T-cell leukemia/lymphoma is associated with activation of Bim and NLRP3


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Title: Induction of apoptosis by HBI-8000 in adult T-cell leukemia/lymphoma is associated with activation of Bim and NLRP3
Authors: Hasegawa, Hiroo / Bissonnette, Reid P. / Gillings, Mireille / Sasaki, Daisuke / Taniguchi, Hiroaki / Kitanosono, Hideaki / Tsuruda, Kazuto / Kosai, Kousuke / Uno, Naoki / Morinaga, Yoshitomo / Imaizumi, Yoshitaka / Miyazaki, Yasushi / Yanagihara, Katsunori
Issue Date: Aug-2016
Publisher: 日本癌学会 / Japanese Cancer Association
Citation: Cancer Science, 107(8), pp.1124-1133; 2016
Abstract: Adult T-cell leukemia/lymphoma (ATL) is an aggressive T-cell malignancy caused by human T-cell lymphotropic virus 1. Treatment options for acute ATL patients include chemotherapy, stem cell transplantation, and recently the anti-chemokine (C-C motif) receptor 4 antibody, although most patients still have a poor prognosis and there is a clear need for additional options. HBI-8000 is a novel oral histone deacetylase inhibitor with proven efficacy for treatment of T-cell lymphomas that recently received approval in China. In the present study, we evaluated the effects of HBI-8000 on ATL-derived cell lines and primary cells obtained from Japanese ATL patients. In most cases HBI-8000 induced apoptosis in both primary ATL cells and cell lines. In addition, findings obtained with DNA microarray suggested Bim activation and, interestingly, the contribution of the NLR family, pyrin domain containing 3 (NLRP3) inflammasome pathway in HBI-8000-induced ATL cell death. Further investigations using siRNAs confirmed that Bim contributes to HBI-8000-induced apoptosis. Our results provide a rationale for a clinical investigation of the efficacy of HBI-8000 in patients with ATL. Although the role of NLRP3 inflammasome activation in ATL cell death remains to be verified, HBI-8000 may be part of a novel therapeutic strategy for cancer based on the NLRP3 pathway.
Keywords: Adult T-cell leukemia lymphoma / apoptosis / Bim / histone deacetylase inhibitors / NLRP3
URI: http://hdl.handle.net/10069/37239
ISSN: 13479032
DOI: 10.1111/cas.12971
Rights: © 2016 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. / This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
Type: Journal Article
Text Version: publisher
Appears in Collections:Articles in academic journal

Citable URI : http://hdl.handle.net/10069/37239

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