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Research Article

setd1a介导的H3K4me3甲基化通过调节WTAPP1/WTAP轴抑制非小细胞肺癌铁下沉

卷 31, 期 21, 2024

发表于: 15 August, 2023

页: [3217 - 3231] 页: 15

弟呕挨: 10.2174/0929867330666230525143252

价格: $65

摘要

介绍：SETD1A在非小细胞肺癌(NSCLC)组织中上调。本研究探讨SETD1A/WTAPP1/WTAP轴在NSCLC中的分子机制。 方法：铁死亡是一种独特的细胞死亡模式，由铁依赖性磷脂过氧化作用驱动，受到多种细胞代谢途径的调节，包括氧化还原稳态、铁代谢、线粒体活性以及氨基酸、脂质和糖的代谢。因此，我们在体外测量了铁凋亡标志物(MDA、SOD、GSH)的水平，并评估了NSCLC细胞的行为。分析setd1a介导的H3K4me3甲基化。在裸鼠模型中验证了setd1a对铁下垂和肿瘤生长的影响。 结果：SETD1A在NSCLC细胞中高表达。沉默SETD1A可抑制NSCLC细胞的增殖和迁移，抑制MDA，提高GPX4、SOD和GSH水平。SETD1A通过介导WTAPP1启动子区域的H3K4me3甲基化，通过上调WTAPP1来提高WTAP的表达。WTAPP1过表达部分避免了沉默SETD1A对NSCLC细胞铁凋亡的促进作用。WTAP干扰消除了WTAPP1对NSCLC细胞铁下垂的抑制作用。沉默SETD1A通过WTAPP1/WTAP轴促进裸鼠铁下垂并加速肿瘤生长。 结论：SETD1A通过介导WTAPP1启动子区域的H3K4me3修饰，通过上调WTAPP1来扩增WTAP的表达，从而促进NSCLC细胞的增殖迁移，抑制铁凋亡。

关键词: 非小细胞肺癌，SETD1A, H3K4me3，表观遗传学，WTAPP1, WTAP，铁下垂。

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