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来自FN14过度表达的BMSCs的外体激活NF-κB信号通路,以诱导骨髓瘤中PANoptosis的发生

Liangming Wang¹, Yanbin Huang¹, Xiaolu Zhang¹

¹Department of Orthopedics, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, 362000, China.

Apoptosis : an international journal on programmed cell death

|January 20, 2025

概括

纤维细胞生长因子可诱导型14 (FN14) 由骨髓介质干细胞的外体提供,通过激活NF-κB信号和触发PANoptosis来抑制骨髓瘤的进展,提供了一种新的治疗策略.

科学领域:

在瘤学瘤学.
细胞生物学细胞生物学
生物化学生物化学

背景情况:

尽管治疗方面取得了进展,骨肉瘤 (OS) 的预后仍然很差,需要新的治疗点.
纤维细胞生长因子诱导型14 (FN14) 涉及各种细胞过程,但其在OS中的作用尚未完全理解.
了解OS瘤微环境中的细胞对细胞通信对于开发有效疗法至关重要.

研究的目的:

研究骨髓介质干细胞 (BMSCs) 和骨干细胞之间的FN14介导通信的作用.
探索FN14载体外体在抑制OS进展中的治疗潜力.
阐明FN14影响OS细胞行为的分子机制.

主要方法:

在正常和OS组织中量化FN14表达.
产生FN14过度表达的BMSC和对外体的隔离 (OE-EXO).
分析OS细胞对外体吸收的情况,高通量测序以阐明机制,以及体内异种移植研究.

主要成果:

在骨组织中观察到FN14表达的减少,与恶性进展相关.
来自BMSCs的FN14丰富外体抑制了OS细胞的增殖和瘤生长 in vivo.
外体体中的FN14激活了NF-κB通路,诱导OS细胞中的PANoptosis.

结论:

通过BMSCs的外体传递的FN14代表了对骨髓瘤的有前途的治疗策略.
针对FN14-NF-κB-PANoptosis轴提供了一种新的方法来对抗OS进展.
通过外体介导的药物递送有可能改善骨髓瘤治疗结果.

关键词:

外基因组是外基因组的组成部分.在FN14/NF-κBB之间.这就是PANoptosis.这就是TWEAKR.瘤微环境是一个微环境.

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