Suppr超能文献

三氧化二砷重塑套细胞淋巴瘤对硼替佐米的反应。

Arsenic trioxide rewires mantle cell lymphoma response to bortezomib.

作者信息

Zhao Ling-Ling, Liu Yuan-Fang, Peng Li-Jun, Fei Ai-Mei, Cui Wen, Miao Sheng-Chao, Hermine Olivier, Gressin Remy, Khochbin Saadi, Chen Sai-Juan, Wang Jin, Mi Jian-Qing

机构信息

State Key Laboratory for Medical Genomics and Department of Hematology, Shanghai Institute of Hematology, Collaborative Innovation Center of Systems Biomedicine, Pôle Sino-Français des Sciences du Vivant et Genomique, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Department of Clinical Laboratory, Shanghai Xuhui Central Hospital, Shanghai, China.

出版信息

Cancer Med. 2015 Nov;4(11):1754-66. doi: 10.1002/cam4.511. Epub 2015 Aug 26.

Abstract

Although most of the mantle cell lymphoma (MCL) patients initially responded well to bortezomib (BTZ), the dose-dependent toxicities have greatly limited the application of BTZ to MCL. To investigate the efficacy and mechanism of arsenic trioxide (ATO) with BTZ in inducing apoptosis of MCL cells, two MCL cell lines, along with primary cells from MCL patients (n = 4), were used. Additionally, the NOD-SCID mice xenograft model of Jeko-1 cells was established to study the anti-MCL mechanisms in an in vivo setting. ATO treatment highly improved BTZ capacity to inhibit proliferation and induce apoptosis of MCL cells. Furthermore, the interaction of Noxa and Mcl-1 leads Bak to release from Mcl-1 or from Bcl-xl, which could further activate Bak and Bax and then induce cell apoptosis. We also found that when lower doses of BTZ were used in combination with ATO, more effective proapoptotic effects in both the cell lines and the primary cells were obtained compared to the effects of BTZ used alone at higher doses. Simultaneously, the combination of these two drugs delayed the tumor growth in mice more effectively than BTZ alone. The cooperative anti-MCL effects of this combination therapy both in vitro and in vivo strongly provided a new strategy to the clinical treatment of MCL.

摘要

尽管大多数套细胞淋巴瘤(MCL)患者最初对硼替佐米(BTZ)反应良好,但剂量依赖性毒性极大地限制了BTZ在MCL中的应用。为了研究三氧化二砷(ATO)联合BTZ诱导MCL细胞凋亡的疗效和机制,使用了两种MCL细胞系以及来自MCL患者的原代细胞(n = 4)。此外,建立了Jeko-1细胞的NOD-SCID小鼠异种移植模型,以在体内研究抗MCL机制。ATO处理显著提高了BTZ抑制MCL细胞增殖和诱导凋亡的能力。此外,Noxa与Mcl-1的相互作用导致Bak从Mcl-1或Bcl-xl中释放出来,这可以进一步激活Bak和Bax,进而诱导细胞凋亡。我们还发现,当低剂量BTZ与ATO联合使用时,与单独使用高剂量BTZ相比,在细胞系和原代细胞中均获得了更有效的促凋亡作用。同时,这两种药物的联合使用比单独使用BTZ更有效地延缓了小鼠肿瘤的生长。这种联合疗法在体外和体内的协同抗MCL作用为MCL的临床治疗强有力地提供了一种新策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a853/4674002/24f63f650987/cam40004-1754-f1.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验