M2巨细胞和瘤细胞参与了代谢反循环,以驱动HCC进展
Yimin Nong1,2, Xiaolong Chen1, Baoxin Zhang2
1Department of Hepatobiliary Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Scientific reports
|November 25, 2025
概括
肝细胞癌 (HCC) 的进展涉及一个代谢-免疫轴,瘤细胞在那里.
科学领域:
- 免疫学 免疫学 免疫学
- 代谢途径 代谢途径
- 癌症生物学 癌症生物学
背景情况:
- 肝细胞癌 (HCC) 因其异质性和免疫抑制性瘤微环境 (TME) 而成为全球健康挑战.
- 与瘤相关的巨细胞 (TAMs),特别是M2极化的巨细胞,通过促进免疫逃避,血管新生和转移,驱动HCC的进展.
- TAM重编程的机制及其在TME内的代谢相互作用尚未完全理解.
研究的目的:
- 在HCC.中识别新的代谢免疫轴.
- 阐明瘤细胞和TAMs之间代谢合的作用.
- 根据代谢和免疫因素开发HCC的预后模型.
主要方法:
- 单细胞RNA测序 (scRNA-seq) 和空间转录组学被用来分析HCC.
- 研究了新陈代谢途径,包括氧化酸化 (OXPHOS) 和巨细胞两极分化.
- 分析了癌症基因组图谱 (TCGA) 数据集,以开发一个预后模型.
主要成果:
- 发现了一种新的代谢-免疫轴,涉及瘤细胞中氧化酸化 (OXPHOS) 的增加和M2巨细胞中的强化核糖体活性.
- 瘤细胞具有高的OXPHOS分泌因素,招募和M2极化巨细胞,加强免疫抑制.
- 基于OXPHOS相关基因的预后模型在多个HCC队列中表现出强大的预测能力.
结论:
- 一个新的OXPHOS-核糖体-M2极化轴显著促进HCC的进展和免疫抑制.
- 这一轴代表了开发HCC新型免疫代谢疗法的潜在治疗目标.
- 瘤细胞中的代谢重编程会影响HCC TME中的巨细胞两极分化和免疫逃避.
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