• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>RSC Advances >The oxidation of (-)-epigallocatechin-3-gallate inhibits T-cell acute lymphoblastic leukemia cell line HPB-ALL via the regulation of Notch1 expression
【24h】

The oxidation of (-)-epigallocatechin-3-gallate inhibits T-cell acute lymphoblastic leukemia cell line HPB-ALL via the regulation of Notch1 expression

机译：（ - ） - EpigallocateChin-3-gallated的氧化抑制T细胞急性淋巴细胞白血病细胞系HPB-所有的调节1

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy, and commonly associated with activating mutations in the Notch1 pathway. (-)-Epigallocatechin-3-gallate (EGCG) is the most abundant and active catechin and has been shown to regulate Notch signaling. Taking into account the highly oxidizable and unstable of EGCG, we proposed that EGCG oxides may have greater potential to regulate Notch signaling than EGCG. In this study, we isolated and identified EGCG oxides (compound 2-4), using a chemical oxidation strategy, and evaluated for cytotoxicity against T-cell acute lymphoblastic leukemia cell line (HPB-ALL) by using the MTS assay. We found compound 3 significantly induced cell proliferation inhibition (38.3858 +/- 1.67106 mu M), cell apoptosis and cell cycle arrest in a dose-dependent manner. Remarkably, compound 3 inhibited expression of Notch1 compared with EGCG in HPB-ALL cells. Meanwhile, we found that compound 3 significantly inhibited c-Myc and Hes1, which are downstream target genes of Notch1. The findings demonstrate for the first time that an oxidation product of EGCG (compound 3) inhibits T-cell acute lymphoblastic leukemia cell line (HPB-ALL) and is a promising agent for cancer therapy deserving further research.
机译：T细胞急性淋巴细胞性白血病（T-ALL）是一个积极的血液恶性肿瘤，以及通常与在Notch1的途径的活化突变相关联。 （ - ） - EpigallocateChin-3-gallate（EGCG）是最丰富和活性的儿茶素，已被证明是调节Notch信号传导。考虑到EGCG的高度可氧化和不稳定，我们提出EGCG氧化物可能具有更大的潜力来调节陷波信号传导而不是EGCG。在该研究中，我们使用化学氧化策略分离和鉴定EGCG氧化物（化合物2-4），并通过使用MTS测定评估针对T细胞急性淋巴细胞白血病细胞系（HPB-All）的细胞毒性。我们发现化合物3显着诱导细胞增殖抑制（38.3858 +/-1.67106μm），细胞凋亡和细胞循环以剂量依赖性方式停留。值得注意地，与HPB-all细胞中的EGCG相比，化合物3抑制了Notch1的表达。同时，我们发现化合物3显着抑制了C-myc和Hes1，其是Notch1的下游靶基因。该研究结果首次证明EGCG（化合物3）的氧化产物抑制T细胞急性淋巴细胞白血病细胞系（HPB-All），并且是癌症治疗的有希望的代理值得进一步的研究。

著录项

  • 来源
    《RSC Advances》 |2020年第3期|共6页
  • 作者

    Wang Yu-Na; Wang Jing; Yang Hao-Nan; Zhang Bang-Lei; Zhang Pan; Sun Pei-Yuan; Zhang Nin; Wang Ya; Sheng Jun; Wang Xuan-Jun; Zi Cheng-Ting;

  • 作者单位

    Yunnan Agr Univ Key Lab Pu Er Tea Sci Minist Educ Kunming 650201 Yunnan Peoples R China;

    Yunnan Agr Univ Key Lab Pu Er Tea Sci Minist Educ Kunming 650201 Yunnan Peoples R China;

    Yunnan Agr Univ Key Lab Pu Er Tea Sci Minist Educ Kunming 650201 Yunnan Peoples R China;

    Yunnan Agr Univ Key Lab Pu Er Tea Sci Minist Educ Kunming 650201 Yunnan Peoples R China;

    Yunnan Agr Univ Key Lab Pu Er Tea Sci Minist Educ Kunming 650201 Yunnan Peoples R China;

    Yunnan Agr Univ Key Lab Pu Er Tea Sci Minist Educ Kunming 650201 Yunnan Peoples R China;

    Yunnan Agr Univ Key Lab Pu Er Tea Sci Minist Educ Kunming 650201 Yunnan Peoples R China;

    Yunnan Agr Univ Key Lab Pu Er Tea Sci Minist Educ Kunming 650201 Yunnan Peoples R China;

    Yunnan Agr Univ Key Lab Pu Er Tea Sci Minist Educ Kunming 650201 Yunnan Peoples R China;

    Yunnan Agr Univ Key Lab Pu Er Tea Sci Minist Educ Kunming 650201 Yunnan Peoples R China;

    Yunnan Agr Univ Key Lab Pu Er Tea Sci Minist Educ Kunming 650201 Yunnan Peoples R China;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 化学;
  • 关键词

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