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抑制SENP3通过调解ESCC进展中的IRF4脱SUMOylation来增强巨细胞的替代激活

Shaoyuan Zhang^1,2, Jianmin Gu^1,2, Wenhan Wang³

¹Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Xuhui District, No. 180, Fenglin Road, Shanghai, 200032, People's Republic of China.

Cell communication and signaling : CCS

|August 9, 2024

概括

这项研究表明,SENP3蛋白调节食道状细胞癌 (ESCC) 中的巨分化. 在巨细胞中较低的SENP3水平与ESCC进展和转移的增加相关.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

食道状细胞癌 (ESCC) 是全球普遍存在的癌症,特别是在东亚.
瘤相关巨细胞 (TAMs) 显著影响ESCC瘤微环境.
蛋白质修饰SUMOylation及其调节剂SUMO特异蛋白酶 (SENPs) 在细胞过程中至关重要.

研究的目的:

调查SENP3在ESCC进展中的作用.
阐明ESCC中SENP3介导的巨细胞极化机制.
在ESCC患者中探索SENP3表达的临床相关性.

主要方法:

从人类ESCC患者的TAM中分析SENP3水平.
使用4-NQO诱导的ESCC小鼠模型研究巨细胞激活.
通过SENP3.3.在K349部位研究干扰素调节因子4 (IRF4) 的脱SUMOylation.
评估巨分化对ESCC细胞迁移,入侵和体内进展的影响.

主要成果:

在人类ESCC患者的TAM中发现SENP3水平上调.
在ESCC小鼠模型中,SENP3的丧失促进了巨细胞的替代激活.
在K349处SENP3de-SUMOylates IRF4,调节巨细胞极化.
替代激活的巨细胞增强了ESCC细胞的迁移,入侵和体内进展.
在巨细胞中SENP3的低表达与更高的PETSUVmax和增加的淋巴结转移相关.

结论:

通过IRF4去SUMOylation,SENP3在调节巨细胞极化方面发挥着至关重要的作用.
通过SENP3介导的巨细胞两极分化影响ESCC的进展和转移.
在TAM中SENP3表达作为ESCC的潜在预后生物标志物.

关键词:

另一个替代激活方式.脱SUMOylation 脱SUMOylation 脱SUMOylation 脱SUMOylation 脱SUMOylation 脱SUMOylation 脱SUMOylation 脱SUMOylation 脱SUMOylation 脱SUMOylation 脱SUMOylation 脱SUMOylation 脱SUMOylation 脱SUMOylation 脱SUMOylation 食管状细胞癌 (ESCC) 是一种在 IRF4 里,你会看到 IRF4.这就是SENP3的意义.这就是SUMOylation的作用.与瘤相关的巨细胞.

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