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TRIM31通过通过ubiquitination修饰保持YBX1蛋白稳定性来触发结直肠癌发生和进展
Xiaoqing Li1,2, Ying Wu3, Jiahao Guo1
1Suzhou Cancer Center Core Laboratory, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Suzhou, China.
Cell death & disease
|August 16, 2025
概括
E3结合酶TRIM31通过稳定YBX1和激活NF-κB驱动结直肠癌. 针对TRIM31可能提供新的结直肠癌疗法.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 生物化学 生化学
背景情况:
- 结肠直肠癌 (CRC) 是一个主要的全球健康问题,其分子驱动因素尚未完全理解.
- 翻译后的蛋白质修改,特别是无处不在,越来越多地被认为是它们在癌症发展中的作用.
研究的目的:
- 研究E3结合酶TRIM31在结直肠癌进展中的作用.
- 阐明TRIM31影响CRC瘤发生的分子机制.
主要方法:
- 评估了CRC组织中的TRIM31表达,并将其与患者预后相关联.
- 采用了体外和体内模型来研究TRIM31对CRC细胞的影响.
- 使用生物化学和分子生物学技术研究了TRIM31,YBX1和NF-κB信号通路之间的相互作用.
主要成果:
- 在CRC中TRIM31的表达很高,并且与预后不佳有关.
- TRIM31的敲击抑制了CRC细胞的增殖,迁移和瘤转移.
- TRIM31通过K63连接的泛化稳定YBX1,增强EREG,GAS6和MAFG的mRNA稳定性.
- TRIM31促进NF-κB (P65) 进入核,创造一个积极的反循环,推动结直肠炎症和致癌.
结论:
- 通过YBX1稳定和NF-κB激活,TRIM31作为结直肠癌发生的关键驱动因素.
- TRIM31代表了结直肠癌干预的潜在治疗标.
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