单细胞转录组学识别了SOCS3+耗尽的T细胞作为促进清细胞细胞癌进展的生物标志物
Xiaoqin Jiang1, Yifan Xu1, Zhenjie Wu1
1Department of Urology, Shanghai Changhai Hospital, Naval Medical University, 168 Changhai Rd, Shanghai, 200433, China.
Clinical and experimental medicine
|November 17, 2025
概括
耗尽的T细胞,特别是SOCS3+耗尽的T细胞,驱动清细胞细胞癌 (ccRCC) 的进展和免疫疗法耐药性. 这些细胞被确定为ccRCC患者的关键预后生物标志物.
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) 是一种常见的癌,早期症状很少.
- 先进的ccRCC可以对免疫疗法做出反应,但进展机制尚未完全理解.
- 耗尽的T细胞与瘤进展和免疫逃避有关.
研究的目的:
- 通过单细胞转录组学,研究耗尽的T细胞在ccRCC进展中的作用.
- 为了确定ccRCC的预后生物标志物.
- 阐明由耗尽的T细胞驱动的免疫逃避机制.
主要方法:
- 使用缩小维度和聚类重新分析单细胞转录组数据.
- 差异基因表达分析以确定预后基因.
- 构建和验证一个名ogram预测模型.
- 基因本体学和Reactome通路丰富分析.
- 用于细胞-细胞通信分析的体受体相互作用概况.
主要成果:
- 确定了九种不同的细胞群,其中SOCS3+耗尽的T细胞显示出显著的预后相关性.
- 一个使用SOCS3和N4BP1的诺莫格拉姆模型准确地将患者分为风险组.
- SOCS3+耗尽的T细胞通过MIF信号通路与髓状细胞相互作用.
- 发现这些细胞促进了对细胞毒性杀伤的抵抗力.
结论:
- 在ccRCC中,SOCS3+耗尽的T细胞促进瘤抵抗细胞毒杀.
- SOCS3+耗尽的T细胞是ccRCC患者强大的预后生物标志物.
- 了解这些细胞为改善ccRCC治疗结果提供了潜在的治疗点.
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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
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