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通过调节E2F1/ATF4轴,ZFP36促进铁和线粒体功能障碍,并通过调节E2F1/ATF4轴抑制骨髓瘤的恶性进展

Shiyue Qin¹, Hongyang Kong², Lei Jiang²

¹Department of Ophthalmology, The Affiliated Taizhou People's Hospital of Nanjing Medical University, Taizhou School of Clinical Medicine, Nanjing Medical University, Taizhou, Jiangsu, 225300, China.

Journal of pharmaceutical analysis

|October 6, 2025

概括

指蛋白36 (ZFP36) 通过促进铁和线粒体功能障碍来抑制骨髓瘤 (OS) 的进展. ZFP36针对E2F1/ATF4通路,为OS治疗提供了一个潜在的治疗策略.

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:

指蛋白36 (ZFP36) 在骨髓瘤 (OS) 组织中下调.
ZFP36在铁和OS发育中的作用需要进一步研究.

研究的目的:

研究ZFP36在骨髓瘤发育过程中调节铁亡的作用和机制.
探索ZFP36作为OS治疗点的潜力.

主要方法:

对OS中差异表达基因 (DEGs) 的基因表达综合 (GEO) 数据集的分析.
西方斑块和免疫组织化学评估ZFP36表达.
用ZFP36过度表达等离子体和siRNAs进行细胞传染.
细胞增殖,迁移和侵入的评估.
测量细胞内Fe2 +,ROS,MDA,GSH,GPX4和SLC7A11水平的测量. 在细胞内测量Fe2 +,ROS,MDA,GSH,GPX4和SLC7A11水平.
线粒体膜潜力 (MMP) 和形态分析.
对E2F1/ATF4信号通路的研究.
使用异种移植小鼠模型进行体内研究.

主要成果:

在OS瘤和细胞系中,ZFP36的下调.
ZFP36过度表达抑制OS细胞的增殖,迁移和入侵.
通过增加Fe2+,ROS,MDA和减少GSH,GPX4,SLC7A11,ZFP36的过度表达促进铁.
过度表达ZFP36会破坏线粒体的功能和形态.
ZFP36促进了E2F1的mRNA降解,而E2F1激活了ATF4的转录.
在体内,ZFP36的过度表达抑制了OS瘤的生长.
E2F1/ATF4轴调解ZFP36对OS进展和铁亡的影响.

结论:

在骨髓瘤中,ZFP36作为瘤抑制剂起作用.
通过调节E2F1/ATF4轴,ZFP36抑制OS进展并促进铁亡.
ZFP36代表了骨髓瘤的一个有前途的治疗标.

关键词:

在ATF4中使用ATF4.E2F1 E2F1 E2F1 E2F1 E2F1 E2F1 E2F1 E2F1 铁化是铁化的一种.线粒体功能障碍线粒体功能障碍骨质肉瘤骨质肉瘤是什么 ZFP36 ZFP36 是一个

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