在ccRCC中,CSF1-CSF1R信号传递介导瘤细胞-巨细胞交叉声和预后
Xing Li1, Yanjun Li1, Lei Zhang1
1Department of Urology, Ningbo Medical Center LiHuiLi Hospital, Ningbo, Zhejiang Province, China.
Cancer gene therapy
|November 27, 2025
概括
向CSF1R可能通过破坏免疫抑制性巨细胞-上皮细胞通信来改善清细胞细胞癌 (ccRCC) 治疗. 这种方法可以提高免疫治疗在癌中的有效性.
科学领域:
- 在瘤学瘤学.
- 免疫学 免疫学 免疫学
- 基因组学就是基因组学.
背景情况:
- 清细胞细胞癌 (ccRCC) 是一种具有不良预后的侵袭性癌,往往是晚诊断的.
- 免疫抑制性瘤微环境 (TME) 和治疗耐药性限制了ccRCC中的免疫治疗疗效.
研究的目的:
- 描述免疫场景,并确定ccRCC TME中的联体受体相互作用.
- 研究CSF1-CSF1R信号在ccRCC进展和免疫抑制中的作用.
主要方法:
- 对ccRCC和正常脏组织的综合单细胞和批量转录组分析.
- 来自公共数据集的基因表达和生存数据的分析.
- 在体内功能验证使用CCRCC异种移植小鼠模型,用CSF1R抑制剂 (Sotuletinib) 治疗.
主要成果:
- 单细胞分析显示,ccRCC中M2型巨细胞和恶性上皮细胞之间的通信增强,由CSF1-CSF1R信号驱动.
- 增加的CSF1和CSF1R表达与预后不佳和巨细胞透增加相关.
- 抑制CSF1R降低了瘤生长,减少了增殖 (Ki67+细胞),并抑制了M2巨细胞极化 (CD163+).
结论:
- 巨细胞和上皮细胞之间的CSF1-CSF1R介导的交叉干涉促进了免疫抑制性TME和ccRCC的进展.
- 准CSF1R提供了一个潜在的策略来调节ccRCC免疫格局并改善治疗结果.
- 对于CellChat预测的配体-受体相互作用,需要进一步的机制验证.
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