TRIP13改变了线粒体功能,并促进了多发性髓瘤中博特佐米布的耐药性
Yang Chen1, Yule Liu2, Yuan Wang3
1Department of Geriatrics, The Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing, People's Republic of China.
Scientific reports
|December 6, 2025
概括
甲状腺激素受体相互作用因子13 (TRIP13) 通过维护线粒体完整性,促进多发性骨髓瘤 (MM) 进展和博特佐米布 (BTZ) 耐药性. 针对TRIP13可能提供一种新的策略,以克服MM患者的BTZ耐药性.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 博尔特佐米布 (BTZ) 耐药性是多发性骨髓瘤 (MM) 治疗的一个重大障碍.
- 了解BTZ耐药性的机制对于开发有效疗法至关重要.
研究的目的:
- 调查甲状腺激素受体交互体13 (TRIP13) 在MM进展中的作用.
- 确定TRIP13在MM中BTZ耐药性的参与.
主要方法:
- 对公共数据集和临床骨髓样本的分析.
- 使用TRIP13过度表达的MM细胞系 (TRIP13-OE) 的体外研究.
- 功能测试,定量聚合酶链反应 (qPCR),共免疫沉和免疫光标签.
主要成果:
- 在MM中,TRIP13是上调调的,与晚期和低生存率相关.
- TRIP13-OE增强了MM细胞的增殖,减少了BTZ诱导的亡,并减轻了细胞循环停止.
- 在BTZ压力下,TRIP13-OE保留了线粒体功能 (膜潜力,水平,ATP产生).
- TRIP13与线粒体单载体 (MCU) 相互作用,这表明它在线粒体调节中的作用.
结论:
- TRIP13在MM进展和BTZ耐药性方面发挥着重要作用.
- 在蛋白质毒性压力下,TRIP13调节线粒体完整性,有助于抵抗.
- 针对 TRIP13 提出了一种潜在的新疗法策略,用于克服MM中BTZ抵抗.
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