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甲胺通过ATF3/NRF2轴调节皮肤皮肤黑色素瘤中的铁亡

Da Gu¹, Yulin Sun², Jianghui Wang³

¹Department of Plastic Surgery, Central Hospital Affiliated to Shandong First Medical University, Jinan, Shandong 250013, PR China.

Cancer genetics

|May 3, 2025

概括

甲胺通过诱导铁亡来抑制皮肤皮肤黑色素瘤 (SKCM) 细胞的增殖. 这通过调节ATF3/NRF2轴来实现,为SKCM提供了潜在的新治疗策略.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
生物化学生物化学

背景情况:

皮肤皮肤黑色素瘤 (SKCM) 是一个重大的健康问题.
目前对SKCM的治疗策略需要新的治疗方法.
了解SKCM进展背后的分子机制至关重要.

研究的目的:

为了研究甲胺对SKCM细胞增殖的影响.
为了确定甲胺是否会在SKCM中诱导铁.
阐明分子机制,特别是ATF3/NRF2轴,涉及甲胺对SKCM的作用.

主要方法:

用CCK-8试验评估细胞增殖.
测量了包括谷氨 (GSH),反应性氧物种 (ROS),脂质过氧化物 (LPO) 和甲 (MDA) 在内的铁灭指标.
RNA测序 (RNA-seq) 确定了差异表达的基因和途径.
西方斑点分析了ATF3和NRF2蛋白质表达.

主要成果:

甲素显著抑制了SKCM细胞的增殖.
甲胺治疗导致GSH降低,ROS,LPO和MDA增加,表明铁灭症诱导.
RNA-seq揭示了基因表达的改变,并激活了与铁代谢和铁灭相关的途径.
甲胺上调了ATF3和下调了NRF2,这表明ATF3/NRF2轴的调节.

结论:

甲胺诱导SKCM细胞中的铁亡.
ATF3/NRF2轴是甲福林抗SKCM作用的关键调解器.
甲胺代表了治疗皮肤皮肤黑色素瘤的潜在新疗法策略.

关键词:

在ATF3中使用ATF3.甲胺是一种甲胺.在RNA-seqqq.铁性化 (ferroptosis) 是一种皮肤皮肤黑色素瘤

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