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Molecular mechanism of methyl jasmonate induced apoptosis in human cancer cells.

机译:茉莉酸甲酯诱导人癌细胞凋亡的分子机制。

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摘要

This study investigated the cytotoxic activity of four plant derived compounds including perillic acid (PA), Perillyl alcohol (POH), cis jasmone (CJ) and methyl jasmonate (MJ) on a variety of human cancer cell lines: Breast (MDA-MB-435, MDA-MB-231, DC4, DB46, T47D, SKBR3 and ZR75-1), Prostate (PC-3 and DU-145) and Lung (A549, H520 and H2170). It was demonstrated that these compounds induce cell cycle arrest and apoptosis by themselves or in combination with other agents. Specifically, MJ decreases membrane fluidity resulting in an activation of tumor necrosis factor receptor 1 (TNFR1) which signals apoptosis via caspase 8 and 2. Combination studies demonstrated that POH, MJ and cisplatin decreased viability, induced cell cycle arrest and activated TNFR1. These results indicate that plant compounds show promise as an alternate treatment option and the combination of these compounds with chemotherapeutic drugs may decrease toxicity and improve efficacy over single agent therapy.
机译:这项研究调查了四种植物衍生化合物(包括紫苏酸(PA),紫苏醇(POH),顺式茉莉酮(CJ)和茉莉酸甲酯(MJ))对多种人类癌细胞系的细胞毒活性:乳腺癌(MDA-MB- 435,MDA-MB-231,DC4,DB46,T47D,SKBR3和ZR75-1),前列腺(PC-3和DU-145)和肺(A549,H520和H2170)。已证明这些化合物本身或与其他试剂组合诱导细胞周期停滞和凋亡。具体而言,MJ降低了膜的流动性,导致肿瘤坏死因子受体1(TNFR1)的激活,该信号通过caspase 8和2发出凋亡信号。联合研究表明,POH,MJ和顺铂降低了活力,诱导了细胞周期停滞并激活了TNFR1。这些结果表明,植物化合物显示出有望作为替代疗法的选择,并且这些化合物与化学治疗药物的组合可降低毒性并提高疗效,优于单药治疗。

著录项

  • 作者

    Yeruva, Venkat Laxmi.;

  • 作者单位

    University of Nevada, Las Vegas.;

  • 授予单位 University of Nevada, Las Vegas.;
  • 学科 Chemistry Biochemistry.;Health Sciences Oncology.
  • 学位 Ph.D.
  • 年度 2007
  • 页码 203 p.
  • 总页数 203
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

  • 入库时间 2022-08-17 11:39:32

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