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SNORD99通过通过2'-O-甲基化修饰来抑制GSDMD介导的烧,促进子宫内膜癌的发展

Jing-Yuan Xian^1,2, Wu Wu^1,2, Xi Chen^1,2

¹Department of Obstetrics and Gynecology, Guangzhou Key Laboratory of Targeted Therapy for Gynecologic Oncology, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.

Journal of cellular and molecular medicine

|October 25, 2024

概括

SNORD99,一个小核细胞RNA,通过抑制热致死,促进子宫内膜癌. 它甲基化GSDMD,抑制细胞死亡和增强瘤生长,表明新的治疗点.

科学领域:

分子生物学分子生物学
细胞生物学细胞生物学
在瘤学瘤学.

背景情况:

细胞具有像热死这样的自我毁灭机制.
小核RNAs (snoRNAs) 可以调节基因表达,并与癌症有关.
热症是一种促炎性编程细胞死亡途径,对免疫和疾病至关重要.

研究的目的:

调查SNORD99在子宫内膜癌 (EC) 病变发生过程中的作用.
阐明SNORD99影响细胞死亡途径的分子机制.
探索SNORD99作为EC的潜在治疗点.

主要方法:

在EC组织中进行SNORD99表达分析的StarBase和qRT-PCR.
细胞增殖,迁移测定和EC细胞中ASO介导的敲击.
RNA测序,RNP复合形成分析,RTL-P,西式斑点和显微镜用于研究SNORD99-GSDMD相互作用和热.

主要成果:

在EC组织中,SNORD99的调节显著提高,并促进了EC细胞的迁移和增殖.
SNORD99过度表达导致了 SNORD99-FBL RNP 复合物的形成,并增加了 GSDMD 2'-O-甲基化.
通过降低GSDMD,caspase-1和NLRP3蛋白质水平,SNORD99抑制了热,从而促进了EC的进展.

结论:

SNORD99通过通过GSDMD 2'-O-甲基化抑制热致死来促进子宫内膜癌的进展.
向SNORD99或增强热致死可能是EC的可行的治疗策略.
这项研究揭示了一种新的机制,将snoRNA与癌症细胞死亡调节联系起来.

关键词:

2'-O-甲基化 2' -O-甲基化 GSDMDMD的总体发展目标是什么这是子宫内膜癌的癌症.热致灭 (pyroptosis) 是一种致的过程.这是一个小核核RNARNA.

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