通过中和CXCL5,可以通过破坏CAF与癌细胞交叉通讯来缓解癌症缓解
Hyun-Jun Kim1, Seon-Wook Kim1, Jun-Hyeong Kim1
1New Drug Targets Laboratory, Department of Life Sciences, College of Life Sciences and Medical Engineering, Gwangju Institute of Science and Technology, Gwangju, Republic of Korea.
Journal of biomedical science
|December 14, 2025
概括
与癌症相关的纤维细胞 (CAFs) 通过分泌CXCL5来驱动缓解症,从而导致肌肉衰竭. 中和CXCL5对癌症患者的肌肉质量保持有希望.
科学领域:
- 在瘤学瘤学.
- 肌肉生物学 肌肉生物学
- 癌症 卡切西亚 病理生理学 癌症
背景情况:
- 严重的骨肌衰竭综合征 - - 症与晚期癌症转移有关,并导致大量癌症相关死亡.
- 目前,没有批准的药物干预措施用于治疗癌症缓解症.
- 与癌症相关的纤维细胞 (CAFs) 参与缓冲症的发展,但它们的确切机制尚不清楚.
研究的目的:
- 阐明癌症关联纤维细胞 (CAFs) 在癌症缓解症的发病过程中的作用.
- 为了确定参与CAF诱导的肌肉消耗的特定分子介质.
- 为了评估向已识别的调解者用于缓解症治疗的治疗潜力.
主要方法:
- 来自CAF和癌症激活CAF的条件介质被用于治疗髓管.
- 在癌症激活的CAF受条件介质中高调的化学激素被使用细胞因子阵列确定.
- 实验室髓管培养物和体内小鼠模型被用于评估化学基因中和的影响.
- 使用体内RNA测序研究了作用机制,并在人体肌肉细胞中验证.
主要成果:
- 癌症激活的CAF诱导了显著的肌管缩,CXCL5被确定为一个关键的上调化学因子.
- 单独CXCL5复制了癌症激活的CAF受条件介质对肌管的缩作用,并抑制了肌源性ERK1/2信号传递.
- 对CXCL5的中和有效地抑制了小鼠模型中的缓解症,并改善了人类神经管中的肌肉损耗.
- RNA测序显示,CXCL5中和促进了与增大相关的信号通路 (PI3K-AKT-MyoG) 并调节了肌肉细胞外基质.
结论:
- 与癌症相关的纤维细胞通过与癌细胞的交叉交互,导致CXCL5分泌量增加,从而导致缓解症.
- CXCL5中和是一种有前途的新型治疗策略,可以在患有缓解症的癌症患者中保持肌肉质量.
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