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首页> 美国卫生研究院文献>Medicina >The Novel Nature Microtubule Inhibitor Ivalin Induces G2/M Arrest and Apoptosis in Human Hepatocellular Carcinoma SMMC-7721 Cells In Vitro
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The Novel Nature Microtubule Inhibitor Ivalin Induces G2/M Arrest and Apoptosis in Human Hepatocellular Carcinoma SMMC-7721 Cells In Vitro

机译：新型自然微管抑制剂伊瓦林诱导人肝癌细胞SMMC-7721细胞的G2 / M逮捕和凋亡。

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Background and Objectives: Microtubules are an attractive target for cancer chemotherapy. Previously, we reported that Ivalin exhibited excellent anti-migration and anti-invasion activities in human breast cancer cells. Here, we examined the microtubule inhibition effect of Ivalin in human hepatocellular carcinoma SMMC-7721 cells. Materials and Methods: We used the 3-(4,5-dimethylthiazol)-2,5-diphenyltetrazolium bromide (MTT) assay to evaluate the cell proliferation effect of Ivalin and flow cytometry analysis to detect the apoptotic and cell cycle arrest effects of Ivalin. Immunofluorescence staining was used to measure the effect of Ivalin on the cytoskeleton network, and Western blotting was used to detect the expression levels of Bax, Bcl-2, Cdc2, phosphor-Cdc2, Cdc25A, Cyclin B1, and tubulin. Results: Ivalin induced cell cycle G2/M arrest and subsequent triggered apoptosis in human hepatocellular carcinoma SMMC-7721 cells. Furthermore, microtubules were shown to be involved in Ivalin-meditated apoptosis. In this connection, Ivalin treatment suppressed cellular microtubule network formation by regulating microtubule depolymerization. Moreover, Western blotting revealed Cdc25A and Cyclin B1 were upregulated in Ivalin-meditated cell cycle arrest. Subsequently, the induction of Bax (a proapoptotic protein) and reduction of Bcl-2 (an anti-apoptotic protein) expression were observed in Ivalin-treated SMMC-7721 cells. Conclusion: Ivalin induced microtubule depolymerization, then blocked cells in mitotic phase, and eventually resulted in apoptosis in SMMC-7721 cells. Collectively, these data indicate that Ivalin, acting as a novel inhibitor of microtubules, could be considered as a promising lead in anticancer drug development.
机译：背景与目的：微管是癌症化疗的诱人靶标。先前，我们报道了伊瓦林在人乳腺癌细胞中表现出出色的抗迁移和抗侵袭活性。在这里，我们检查了伊瓦林在人肝细胞癌SMMC-7721细胞中的微管抑制作用。材料和方法：我们使用3-（4,5-二甲基噻唑）-2,5-二苯基四唑溴化物（MTT）分析评估伊瓦林的细胞增殖作用，并使用流式细胞术分析检测伊伐林的凋亡和细胞周期阻滞作用。免疫荧光染色用于测定伊瓦林对细胞骨架网络的影响，蛋白质印迹用于检测Bax，Bcl-2，Cdc2，荧光体Cdc2，Cdc25A，细胞周期蛋白B1和微管蛋白的表达水平。结果：Ivalin诱导人肝癌SMMC-7721细胞的G2 / M周期阻滞并随后触发凋亡。此外，显示微管参与了伊伐林介导的细胞凋亡。就此而言，伊瓦林治疗通过调节微管解聚作用抑制了细胞微管网络的形成。此外，Western印迹显示，在Ivalin参与的细胞周期停滞中，Cdc25A和Cyclin B1上调。随后，在用伊伐林处理的SMMC-7721细胞中观察到了Bax（促凋亡蛋白）的诱导和Bcl-2（抗凋亡蛋白）表达的降低。结论：伊瓦林诱导微管解聚，然后阻止细胞进入有丝分裂期，最终导致SMMC-7721细胞凋亡。总体而言，这些数据表明，伊瓦林，作为微管的新型抑制剂，可以被认为是抗癌药物开发的有希望的先导。

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