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在前列腺癌中,SETD7通过甲基化FOXA1来作为转录抑制剂起作用

Zifeng Wang^1,2, Jessica Petricca^3,4, Mingyu Liu^1,2

¹Center for Personalized Cancer Therapy, University of Massachusetts Boston, Boston, MA 02125.

Proceedings of the National Academy of Sciences of the United States of America

|August 7, 2023

概括

通过甲基化FOXA1,SETD7作为割抵抗性前列腺癌 (CRPC) 的瘤抑制剂,破坏其功能. 失去SETD7表达与侵袭性前列腺癌相关,突出其在疾病进展中的抑制作用.

科学领域:

表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
分子瘤学分子瘤学
前列腺癌研究研究前列腺癌研究

背景情况:

基因组修饰剂的失调驱动了割抵抗性前列腺癌 (CRPC) 的表观遗传变化.
LSD1去甲基化FOXA1,稳定其染色质结合并增强前列腺癌 (PCa) 中的瘤转录.
负责FOXA1甲基化和FOXA1-LSD1轴的负调节的甲基转移酶是未知的.

研究的目的:

确定向FOXA1-K270的甲基转移酶,并阐明其在CRPC中的作用.
调查SETD7作为甲基转移酶在PCa进展中的非希斯基质,特别是FOXA1上的功能.

主要方法:

研究了SETD7作为向CRPC细胞中的FOXA1-K270的甲基转移酶的作用.
评估了SETD7对FOXA1介导转录及其在PCa细胞中的瘤抑制活性的影响.
与PCa进展和瘤攻击性相关的SETD7表达水平.

主要成果:

在CRPC细胞中,SETD7作为FOXA1-K270的主要甲基转移酶,作为转录抑制剂.
SETD7甲基化破坏FOXA1介导的转录,赋予PCa细胞中的瘤抑制活性.
失去SETD7表达与晚期PCa和瘤攻击性增加显著相关.

结论:

在PCa中,SETD7通过甲基化FOXA1-K270作为瘤抑制剂,从而抑制瘤转录.
SETD7的瘤抑制和转录抑制活动对于调解PCa进展和治疗耐药性至关重要.
了解SETD7-FOXA1相互作用为CRPC中的表观遗传调节提供了机制性的洞察力.

关键词:

我们的FOXA1A1 一个LSD1一个LSD1 在SETD7中,SETD7是SETD7.溶氨酸甲基化溶氨酸甲基化前列腺癌是前列腺癌.

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