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首页> 外文期刊>Anticancer Research: International Journal of Cancer Research and Treatment >Synergistic Cytotoxicity of Bendamustine and the BTK Inhibitor in a Mantle Cell Lymphoma Cell Line
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Synergistic Cytotoxicity of Bendamustine and the BTK Inhibitor in a Mantle Cell Lymphoma Cell Line

机译：弯蛋白蛋白和BTK抑制剂的协同细胞毒性伴细胞细胞淋巴瘤细胞系

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Background: Bendamustine is effective in B-cell malignancies, including mantle cell lymphoma (MCL), alone and in combination with other agents. This study investigated the combination effect of bendamustine and the Bruton tyrosine kinase (BTK) inhibitor PCI-32765 on MCL cell death and the underlying mechanisms. Materials and Methods: Cytotoxicity was examined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MIT) assay. Apoptosis was assessed by annexin V/propidium iodide staining and protein expression was analyzed by western blotting. Results: When combined with bendamustine, PCI-32765 showed a synergistic effect on growth inhibition of the MCL cell line Jeko-1. Cleavage of caspase-3 and poly-(ADP-ribose) polymerase was increased, indicating enhanced apoptosis induction. In addition, this combination decreased the protein expression of cyclin D1. Phosphorylated v-akt murine thymoma viral oncogene homolog 1 (AKT) (Ser473) was also down-regulated, suggesting a suppression of the phosphatidylinositol 3-kinase/AKT signaling pathway. Conclusion: Combination treatment with bendamustine and a BTK inhibitor may be effective in MCL therapy.
机译：背景：Bendamustine在B细胞恶性肿瘤中是有效的，包括地幔细胞淋巴瘤（MCL），单独和与其他药剂组合。本研究研究了弯曲蛋白和沥青酪氨酸激酶（BTK）抑制剂PCI-32765对MCL细胞死亡和潜在机制的组合效应。材料和方法：通过3-（4,5-二甲基噻唑-2-基）-2,5-二苯基四唑烷铵（MIT）测定检查细胞毒性。通过膜蛋白v /碘化丙啶染色来评估细胞凋亡，并通过Western印迹分析蛋白质表达。结果：与弯曲蛋白结合时，PCI-32765对MCL细胞系JEKO-1的生长抑制表现出协同作用。增加了Caspase-3和聚 - （ADP-核糖）聚合酶的切割，表明增强的凋亡诱导。此外，这种组合降低了细胞周期蛋白D1的蛋白质表达。磷酸化的V-AKT鼠胸腺瘤病毒癌基因同源物1（AKT）（AKT）（SER473）也被下调，表明抑制磷脂酰肌醇3-激酶/ AKT信号通路。结论：用弯曲蛋白和BTK抑制剂的组合治疗在MCL治疗中可能是有效的。

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