Tabe Yoko, Kojima Kensuke, Yamamoto Shinichi, Sekihara Kazumasa, Matsushita Hiromichi, Davis Richard Eric, Wang Zhiqiang, Ma Wencai, Ishizawa Jo, Kazuno Saiko, Kauffman Michael, Shacham Sharon, Fujimura Tsutomu, Ueno Takashi, Miida Takashi, Andreeff Michael
Section of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas M. D. Anderson Cancer Center, Houston, TX, United States of America; Department of Clinical Laboratory Medicine, Biomedical Research Center Graduate School of Medicine, Juntendo University, Tokyo, Japan.
Section of Molecular Hematology and Therapy, Department of Leukemia, The University of Texas M. D. Anderson Cancer Center, Houston, TX, United States of America.
PLoS One. 2015 Sep 4;10(9):e0137210. doi: 10.1371/journal.pone.0137210. eCollection 2015.
Mantle cell lymphoma (MCL) is an aggressive B-cell lymphoma characterized by the aberrant expression of several growth-regulating, oncogenic effectors. Exportin 1 (XPO1) mediates the nucleocytoplasmic transport of numerous molecules including oncogenic growth-regulating factors, RNAs, and ribosomal subunits. In MCL cells, the small molecule KPT-185 blocks XPO1 function and exerts anti-proliferative effects. In this study, we investigated the molecular mechanisms of this putative anti-tumor effect on MCL cells using cell growth/viability assays, immunoblotting, gene expression analysis, and absolute quantification proteomics. KPT-185 exhibited a p53-independent anti-lymphoma effect on MCL cells, by suppression of oncogenic mediators (e.g., XPO1, cyclin D1, c-Myc, PIM1, and Bcl-2 family members), repression of ribosomal biogenesis, and downregulation of translation/chaperone proteins (e.g., PIM2, EEF1A1, EEF2, and HSP70) that are part of the translational/transcriptional network regulated by heat shock factor 1. These results elucidate a novel mechanism in which ribosomal biogenesis appears to be a key component through which XPO1 contributes to tumor cell survival. Thus, we propose that the blockade of XPO1 could be a promising, novel strategy for the treatment of MCL and other malignancies overexpressing XPO1.
套细胞淋巴瘤(MCL)是一种侵袭性B细胞淋巴瘤,其特征在于几种生长调节致癌效应因子的异常表达。核输出蛋白1(XPO1)介导包括致癌生长调节因子、RNA和核糖体亚基在内的众多分子的核质运输。在MCL细胞中,小分子KPT-185可阻断XPO1功能并发挥抗增殖作用。在本研究中,我们使用细胞生长/活力测定、免疫印迹、基因表达分析和绝对定量蛋白质组学,研究了这种假定的对MCL细胞的抗肿瘤作用的分子机制。KPT-185通过抑制致癌介质(如XPO1、细胞周期蛋白D1、c-Myc、PIM1和Bcl-2家族成员)、抑制核糖体生物合成以及下调作为热休克因子1调控的翻译/转录网络一部分的翻译/伴侣蛋白(如PIM2、EEF1A1、EEF2和HSP70),对MCL细胞表现出不依赖p53的抗淋巴瘤作用。这些结果阐明了一种新机制,其中核糖体生物合成似乎是XPO1促进肿瘤细胞存活的关键组成部分。因此,我们提出阻断XPO1可能是治疗MCL和其他过表达XPO1的恶性肿瘤的一种有前景的新策略。