通过Nrf2信号通路在结肠直肠癌细胞中诱导铁亡的氧铁醇
Weipeng Li1,2,3, Yangyang Li1,2,3, Fengchi Lin1,2,3
1Translational Medicine Research Center, Sun Yat-sen University Cancer Center Gansu Hospital, Lanzhou, 730050, Gansu, China.
Scientific reports
|July 2, 2025
概括
氧醇 (HT) 通过激活Nrf2信号通路,诱导结直肠癌细胞的细胞死亡过程 - - 铁亡. 这一发现为治疗耐药结直肠癌提供了潜在的新策略.
科学领域:
- 在瘤学瘤学.
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 结肠直肠癌的发病率正在上升,目前的治疗方法由于瘤细胞的抵抗性而面临限制.
- 铁亡,一种独特的编程细胞死亡形式,为克服癌症治疗耐药性的有希望的途径.
- 氧醇 (HT) 正在研究其潜在的抗瘤特性.
研究的目的:
- 阐明氧醇 (HT) 在结直肠癌细胞中诱导铁亡的机制.
- 为了研究核因子-红素2相关因子2 (Nrf2) 信号通路在HT介导的铁亡中的作用.
- 通过网络药理学和分子对接,识别和确认结直肠癌治疗的HT目标.
主要方法:
- 网络药理学和分子对接被用来识别HT的潜在目标.
- 细胞活力,殖民地形成和划伤试验评估了结直肠癌细胞对HT的反应.
- 西方涂抹和光探针技术被用来分析分子变化.
主要成果:
- 网络药理学确定了14个核心目标,其中Nrf2被确定为主要目标.
- 分子对接证实HT与氧化应激相关的标结合,包括Nrf2,NQO1,TrxR1,PTGS2和AKR1C3.3.
- HT治疗增加了铁含量,脂质过氧化和活性氧物种,同时降低了谷氨和线粒体膜潜能,这表明铁亡.
结论:
- 氧醇 (HT) 在结直肠癌细胞中有效诱导铁.
- Nrf2信号通路是HT诱导铁亡的关键调解者.
- HT显示出作为结直肠癌治疗剂的潜力,特别是在克服耐药性方面.
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