库普弗细胞衍生IL6通过JAK1-ACAP4途径促进肝细胞癌转移
Tao Li1, Xiaoyu Song2, Jiena Chen3
1School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, 100029, China.
International journal of biological sciences
|January 2, 2025
概括
肝细胞癌 (HCC) 细胞通过外体促进肝脏库弗弗细胞 (KCs) 通过外体成为瘤相关巨细胞 (TAMs). 这种IL6-JAK1-ACAP4通路驱动HCC转移,但布法林通过抑制JAK1.1显示治疗潜力.
科学领域:
- 肝胆道癌症 肝胆道癌症
- 癌症免疫学 癌症免疫学
- 细胞信号传递 细胞信号传递
背景情况:
- 与瘤相关的巨细胞 (TAMs) 影响癌症的进展.
- 库普弗细胞 (KC) 在肝细胞癌 (HCC) 中的作用尚未完全理解.
研究的目的:
- 阐明HCC细胞与KCs相互作用的机制.
- 为了确定HCC转移的治疗点.
主要方法:
- 从HCC细胞中对外体隔离和表征.
- 对IL6-JAK1-ACAP4信号轴的分析.
- 在体外和体内测试细胞迁移和转移.
- 查布法林的治疗潜力.
主要成果:
- 由HCC衍生的外体诱导KCs分化为TAMs.
- IL6-JAK1-ACAP4轴介导HCC细胞迁移和转移.
- 在HCC患者组织中IL6,p-JAK1和p-ACAP4水平升高.
- 布法林抑制了JAK1,阻断了ACAP4的酸化,并减少了HCC的转移.
结论:
- HCC细胞通过外体促进KC转化为TAM,通过IL6-JAK1-ACAP4轴驱动转移.
- IL6-JAK1-ACAP4轴是HCC的潜在治疗点.
- 布法林通过抑制JAK1.1,对HCC具有治疗潜力.
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