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通过SETDB1介导的CD147-K71二甲基化促进非小细胞肺癌中细胞亡

Ming-Yan Shi¹, Yarong Wang¹, Ying Shi¹

¹National Translational Science Center for Molecular Medicine & Department of Cell Biology, Fourth Military Medical University, Xi'an, Shaanxi 710032, China.

Genes & diseases

|September 11, 2023

概括

CD147二甲基化 (CD147-K71me2) 抑制非小细胞肺癌 (NSCLC) 的进展. 这种翻译后的修改促进了FOSB表达,并增强了p38酸化,导致瘤细胞亡.

科学领域:

分子生物学分子生物学
癌症研究癌症研究
生物化学生物化学

背景情况:

蛋白质后翻译性修饰 (PTMs) 调节细胞信号传递,并与瘤进展有关.
瘤生物标志物CD147通过各种PTMs影响转移和代谢.
CD147 PTMs在亡中的作用在很大程度上仍未被探索.

研究的目的:

研究非小细胞肺癌 (NSCLC) 中的CD147翻译后修饰和亡之间的关系.
为了确定特定的CD147修饰及其在瘤进展中的功能后果.

主要方法:

开发一种针对CD147 K71二甲基化 (CD147-K71me2) 的特定抗体.
在NSCLC组织中分析CD147-K71me2水平.
使用RNA-seq和分子测定方法识别甲基转移酶 (SETDB1) 和下游目标 (FOSB,p38酸化).
在体内瘤进展研究.

主要成果:

与相邻组织相比,NSCLC组织中的CD147-K71me2水平较低.
SETDB1被确定为负责CD147-K71me2.2的甲基转移酶.
发现CD147-K71me2通过增强的p38酸化促进FOSB表达,诱导瘤细胞亡.
在体内实验中,通过诱导亡,CD147-K71me2显著抑制了瘤进展.

结论:

CD147-K71me2在瘤进展中起着抑制作用,与CD147.7的促癌功能不同.
这项研究扩大了对CD147在癌症中的作用的理解,强调了其翻译后修饰对亡的影响.

关键词:

在CD147二甲基化中.细胞亡是细胞的亡.这就是FOSB.非小细胞肺癌是非小细胞肺癌.在SETDB1中,我们可以使用SETDB1.

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