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环林J限制了线性无素信号传递,并控制了结直肠癌的进展

Chunjie Sheng¹, Chen Yao¹, Jing Wang¹

¹State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, PR China.

The Journal of biological chemistry

|July 29, 2024

概括

环林J (CYPJ) 通过抑制线性无素链合成来抑制炎症和癌症,这是NF-κB通路的关键激活剂. 缺少CYPJ增加了对结肠炎和结肠癌的易感性,而其表达与患者更好的存活率相关.

科学领域:

分子生物学分子生物学
免疫学免疫学免疫学
在瘤学瘤学.

背景情况:

慢性炎症通过过度的核因子kappa-B (NF-κB) 信号传递驱动肠胃癌,如结直肠癌.
线性泛素链对于激活正规NF-κB通路至关重要.
线性ubiquitin链组合复合体 (LUBAC) 合成这些链,促进炎症和癌症.

研究的目的:

为了确定线性无素链组合复合体 (LUBAC) 的负调节者.
调查环菲林J (CYPJ) 在调节NF-κB信号和炎症驱动的瘤发生中的作用.

主要方法:

研究了CYPJ与LUBAC组件 (HOIL-1相互作用蛋白和Shank相关的RH域相互作用蛋白) 的相互作用.
评估了CYPJ缺乏对硫酸诱导的大肠炎和氧甲诱导的小鼠结肠癌的影响.
分析了与患者生存结果相关的CYPJ和缺氧诱导因子-1α (HIF-1α) 表达.

主要成果:

CYPJ直接与LUBAC成分结合,破坏它们的相互作用,并抑制线性无素链合成和NF-κB激活.
缺乏Cypj的小鼠对结肠炎和结肠癌的易感性增加.
增加CYPJ表达,特别是在低氧条件下 (由HIF-1α诱导),与癌症患者的整体和无进展生存率的改善相关.

结论:

CYPJ作为LUBAC的新型负调节剂,减轻炎症并抑制炎症驱动的瘤发生.
在预防结肠炎和结肠癌方面,CYPJ对NF-κB信号的抑制作用至关重要.
CYPJ代表了管理炎症性疾病和相关癌症的潜在治疗标.

关键词:

在CRC中,CRC就是CRC.在CYPJ中.卢巴克 (Lubac) 的一个地方.在 NF-κBB 中.线性无处不在的线性

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