解读衰老和泛癌的联系:单细胞测序揭示了微环境重塑和细胞驱动因素
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Updated: Jan 14, 2026

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Published on: May 26, 2023
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Yue Han1, Nuo Chen1, Ping Wang1
1Department of Dermatology, The Union Hospital, Fujian Medical University, Fuzhou, Fujian, China.
Bioscience trends
|October 26, 2025
概括
老龄化显著增加了癌症的风险. 衰老细胞随着年龄的增长而积累,通过改变瘤微环境和削弱免疫力,促进瘤生长和转移. 老化疗法在治疗与年龄相关的癌症方面表现有前途.
科学领域:
- 在瘤学瘤学.
- 免疫学 免疫学 免疫学
- 衰老研究研究 衰老研究
背景情况:
- 衰老是癌症的主要风险因素,60%的恶性瘤发生在65岁以上的人身上.
- 衰老细胞积聚在老化的组织中,导致基因组不稳定,并分泌出促瘤原生因素.
- 免疫衰变会损害抗瘤免疫力,增加对癌症的易感性.
研究的目的:
- 审查老化如何重编程瘤微环境 (TME) 以促进癌症发生.
- 探索衰老细胞及其相关分泌表型 (SASP) 在癌症进展中的作用.
- 确定与癌症存活率差相关的保存的衰老基因特征,并讨论治疗策略.
主要方法:
- 分析来自TCGA和GEO等数据库的单细胞RNA测序 (scRNA-seq) 数据.
- 陈旧细胞亚种群及其分泌因子 (SASP) 的分析.
- 全癌症分析衰老基因特征及其与患者存活率的相关性.
主要成果:
- 衰老细胞 (例如CDKN2A+/LMNB1-) 在老化的组织中累积高达15%,导致不稳定性和分泌SASP因子 (IL-6,TGF-β).
- SASP因子重塑TME,在小鼠模型中增加纤维细胞激活和转移40-70%.
- 免疫发生导致耗尽的T细胞和免疫抑制性髓状细胞的增加;衰老特征与30-50%的生存率相对应.
结论:
- 衰老通过TME重编程,衰老细胞积累和免疫抑制促进癌症.
- 在临床前试验中,解策略显示出潜力,在临床前试验中改善药物反应3.5倍.
- 整合多学科和人工智能对于开发针对衰老相关癌症的向疗法至关重要.
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