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通过调节H3K27me3介导的PEBP1/Raf-1/MEK/ERK MAPK信号,PRDM14促进了NSCLC细胞的增殖,迁移和侵入

He Shi¹, Yunfei Jiang², Haijun Mu²

¹Medical Laboratory Center of Hangzhou Hospital of Traditional Chinese Medicine, Hangzhou, China.

Genes & genomics

|August 26, 2025

概括

通过H3K27me3修饰,PRDM14通过激活PEBP1/Raf-1/MEK/ERK通路促进非小细胞肺癌 (NSCLC) 的生长和转移. 这一发现表明PRDM14是NSCLC的潜在治疗点.

科学领域:

癌症学
分子生物学
表观遗传学

背景情况:

之前的研究发现PRDM14是非小细胞肺癌 (NSCLC) 细胞迁移的促进者.
推动PRDM14在NSCLC中的转移性作用的基本分子机制在很大程度上仍未被阐明.

研究的目的:

研究PRDM14在NSCLC细胞增殖和转移中的作用.
阐明涉及的信号通路,特别关注PEBP1/Raf-1/MEK/ERK信号的H3K27me3介导调节.

主要方法:

使用过度表达等离子体和siRNA操纵PRDM14和JMJD3的表达.
使用Vemurafenib (VMF) 抑制Raf-1/MEK/ERK通路.
通过EDU染色,殖民地形成和跨井检测评估细胞增殖,迁移和入侵.
通过西式涂抹和qPCR量化关键信号分子 (PRC2,H3K27me3,PEBP1,Raf-1/MEK/ERK通路组成部分) 的蛋白质和mRNA水平.

主要成果:

PRDM14的过度表达增强了NSCLC细胞的增殖,迁移和侵袭,与PRC2和H3K27me3的增加相关,PEBP1的减少,并激活了Raf-1/MEK/ERK信号.
对于PRDM14的抗击作用相反.
韦穆拉非尼部分逆转了PRDM14对细胞功能和信号的作用,但没有改变PEBP1或H3K27me3水平.
抑制JMJD3增强了PRDM14的抗瘤作用

结论:

通过PRC2/H3K27me3介导的表观遗传修饰,PRDM14通过激活PEBP1/Raf-1/MEK/ERK通路来驱动NSCLC的进展.
在NSCLC治疗中,PRDM14是一个有前途的治疗点.

关键词:

H3K27me3 其他含有Jumonji域的蛋白质3 非小细胞肺癌在 PEBP1/Raf-1/MEK/ERK MAPK 信号中含有蛋白质的PRDI-BF1和RIZ同质域多镇压复合体2

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