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细胞系依赖的细胞死亡途径诱导的thymoquinone在结肠直肠癌细胞.

Natalia Kurowska1, Maria Książek1, Paulina Borkowska2

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概括

蒂莫金 (TQ) 通过不同的细胞死亡途径减少结直肠癌 (CRC) 细胞活力,这取决于癌症.

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科学领域:

  • 在瘤学瘤学.
  • 分子生物学分子生物学
  • 药理学 药理学是指药理学的学科.

背景情况:

  • 大肠直肠癌 (CRC) 是癌症死亡的主要原因.
  • 对5-甲 (5-FU) 的耐药性是CRC治疗中的一个重要治疗障碍.
  • 来自Nigella sativa的提摩 (TQ) 显示出抗癌潜力,但其细胞死亡机制取决于上下文.

研究的目的:

  • 在结直肠癌模型中研究TQ诱导的细胞系特异性死亡途径.
  • 为了比较TQ对5-FU敏感 (RKO) 和5-FU抗性 (SW1116) CRC细胞系的影响.
  • 评估TQ对正常结肠上皮细胞的影响.

主要方法:

  • 细胞活力测试 (MTT)
  • 对DNA碎片化分析进行分析.
  • 卡斯巴酶活性测定 (卡斯巴酶-3/7, -8, -9)
  • 细胞死亡表型分析 (流细胞计)
  • 对亡和亡标记物的基因表达分析 (RT-qPCR).

主要成果:

  • 在RKO和SW1116细胞中,TQ降低了活力,对正常细胞的毒性最小.
  • 在RKO细胞 (微卫星不稳定性) 中,TQ通过卡斯巴酶激活和亲细胞灭绝基因上调诱导了亡.
  • 在SW1116细胞 (染色体不稳定性) 中,TQ触发了独立于酶的死细胞死亡.
  • 结合TQ和5-FU治疗没有显示出协同性细胞毒性,但有明显的细胞死亡程序.

结论:

  • TQ通过上下文依赖的机制诱导癌细胞死亡,主要是MSI细胞的亡和CIN细胞的亡.
  • TQ的有效性是由结直肠癌细胞的分子背景调节的.
  • TQ不会协同增强5-FU的有效性,但会激活不同的细胞死亡途径.