CXCL8/SDC1轴调解瘤干细胞相互作用,以驱动甲状腺癌的远程转移
Wenjuan Wang1, Jian Zhou2, Baorui Tao2
1Department of Pathology, Huashan Hospital, Fudan University, Shanghai, 200040, China.
Journal of pharmaceutical analysis
|February 2, 2026
概括
研究人员确定CXCL8 / SDC1轴对甲状腺癌 (THCA) 转移至关重要. 单细胞和瘤干细胞之间的这种相互作用激活了JAK-STAT信号,推动了癌症的进展,并表明THCA患者的预后不佳.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 免疫学 免疫学 免疫学
背景情况:
- 甲状腺癌 (THCA) 转移仍然是一个重大挑战.
- 了解THCA远程传输的分子驱动因素对于改善患者的治疗结果至关重要.
研究的目的:
- 阐明THCA远程传输背后的分子机制.
- 为了研究C-X-C动机化学因配体8 (CXCL8) 阳性单细胞和syndecan-1 (SDC1) 阳性瘤干细胞之间的相互作用.
主要方法:
- 单细胞和THCA患者样本的空间转录组测序.
- 使用Seurat,CellChat和SPOTlight R软件包进行生物信息分析.
- 在小鼠体外共培系统,ELISA,西式涂抹和体内异种/转移模型.
主要成果:
- 鉴定出CXCL8/SDC1轴是Janus酶信号转换器和转录激活器 (JAK-STAT) 信号传输的关键调解器.
- 这个轴促进THCA干细胞的自我更新,入侵和转移.
- 高CXCL8/SDC1表达与高风险C1亚型相关,THCA患者的预后较差.
结论:
- CXCL8阳性单细胞和SDC1阳性瘤干细胞的相互作用激活了JAK-STAT通路,促进了THCA转移.
- 针对CXCL8/SDC1轴为THCA提供了一个潜在的治疗策略.
- 这个轴是预测THCA患者预后的有希望的生物标志物.
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