...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cellular Physiology and Biochemistry >Magnolol Inhibits the Growth of Non-Small Cell Lung Cancer via Inhibiting Microtubule Polymerization
【24h】

Magnolol Inhibits the Growth of Non-Small Cell Lung Cancer via Inhibiting Microtubule Polymerization

机译：厚朴酚通过抑制微管聚合来抑制非小细胞肺癌的生长

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

>Background: The tubulin/microtubule system, which is an integral component of the cytoskeleton, plays an essential role in mitosis. Targeting mitotic progression by disturbing microtubule dynamics is a rational strategy for cancer treatment. Methods: Microtubule polymerization assay was performed to examine the effect of Magnolol (a novel natural phenolic compound isolated from Magnolia obovata) on cellular microtubule polymerization in human non-small cell lung cancer (NSCLC) cells. Cell cycle analysis, mitotic index assay, cell proliferation assay, colony formation assay, western blotting analysis of cell cycle regulators, Annexin V-FITC/PI staining, and live/dead viability staining were carried out to investigate the Magnolola€?s inhibitory effect on proliferation and viability of NSCLS cells in vitro. Xenograft model of human A549 NSCLC tumor was used to determine the Magnolola€?s efficacy in vivo. Results: Magnolol treatment effectively inhibited cell proliferation and colony formation of NSCLC cells. Further study proved that Magnolol induced the mitotic phase arrest and inhibited G2/M progression in a dose-dependent manner, which were mechanistically associated with expression alteration of a series of cell cycle regulators. Furthermore, Magnolol treatment disrupted the cellular microtubule organization via inhibiting the polymerization of microtubule. We also found treatment with NSCLC cells with Magnolol resulted in apoptosis activation through a p53-independent pathway, and autophgy induction via down-regulation of the Akt/mTOR pathway. Finally, Magnolol treatment significantly suppressed the NSCLC tumor growth in mouse xenograft model in vivo. Conclusion: These findings identify Magnolol as a promising candidate with anti-microtubule polymerization activity for NSCLC treatment.
机译：> 背景： 微管蛋白/微管系统是细胞骨架的组成部分，在有丝分裂中起着至关重要的作用。通过干扰微管动力学来靶向有丝分裂进程是治疗癌症的合理策略。 方法： 进行微管聚合试验以检测木兰醇（木兰厚朴分离的新型天然酚类化合物）对人非小细胞肺癌细胞微管聚合的影响（NSCLC）细胞。进行了细胞周期分析，有丝分裂指数测定，细胞增殖测定，集落形成测定，细胞周期调节剂的蛋白质印迹分析，膜联蛋白V-FITC / PI染色和活/死活力染色，以研究木兰醇的抑制作用对NSCLS细胞的体外增殖和活力的影响。使用人类A549 NSCLC肿瘤的异种移植模型确定Magnolola的体内功效。 结果： 厚朴酚处理可有效抑制NSCLC细胞的增殖和集落形成。进一步的研究证明，厚朴酚以剂量依赖的方式诱导了有丝分裂期阻滞并抑制了G2 / M的进程，这与一系列细胞周期调节因子的表达改变在机制上相关。此外，厚朴酚处理通过抑制微管的聚合而破坏了细胞的微管组织。我们还发现，用Magnolol处理NSCLC细胞可通过不依赖p53的途径激活凋亡，并通过下调Akt / mTOR途径进行自噬诱导。最后，在小鼠体内异种移植模型中，厚朴酚治疗显着抑制了NSCLC肿瘤的生长。 结论： 这些发现确定了Magnolol是具有抗微管聚合活性的NSCLC治疗的有希望的候选者。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号