CD81 通过阻断 CD274/PD-L1 的选择性自噬降解驱动放射抵抗性胶质母细胞瘤的免疫逃逸
CD81 drives immune evasion in radioresistant glioblastoma by blocking selective autophagic degradation of CD274/PD-L1.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
肿瘤干细胞与肿瘤相关巨噬细胞：相互作用及治疗机会
英文原题：Cancer stem cells and tumor-associated macrophages: Interactions and therapeutic opportunities.
查看英文原题
Cancer stem cells and tumor-associated macrophages: Interactions and therapeutic opportunities.
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中文摘要
癌症干细胞（CSCs）依赖肿瘤微环境（TME）通过招募单核细胞并将其重编程为肿瘤相关巨噬细胞（TAMs）来维持其干性特性，而TAMs反过来促进肿瘤进展。本综述探讨了CSC-TAM相互作用，强调CSCs如何驱动单核细胞招募和TAM极化。我们讨论了TAMs如何通过趋化因子、细胞因子、外泌体介导的miRNA转移、直接相互作用以及细胞外基质（ECM）重塑来增强CSC干性和龛维持。此外，我们审视了靶向TAMs的治疗策略，包括抑制TAM分化、重编程TAM极化，以及利用免疫检查点阻断和CAR-巨噬细胞免疫疗法来改善癌症治疗结果。
展开英文摘要原文
Cancer stem cells (CSCs) depend on the tumor microenvironment (TME) to sustain their stem-like properties by recruiting monocytes and reprogramming them into tumor-associated macrophages (TAMs), which in turn promote tumor progression. This review explores CSC-TAM interactions, emphasizing how CSCs drive monocyte recruitment and TAM polarization.
We discuss how TAMs enhance CSC stemness and niche maintenance through chemokines, cytokines, exosome-mediated miRNA transfer, direct interactions, and extracellular matrix (ECM) remodeling.
Furthermore, we examine therapeutic strategies targeting TAMs, including inhibiting TAM differentiation, reprogramming TAM polarization, and leveraging immune checkpoint blockade and CAR-macrophage immunotherapy to improve cancer treatment outcomes.
论文信息
- 作者
- Yuan H、Qiu Y、Mei Z、Liu J、Wang L、Zhang K、Liu H、Zhu F
- 第一作者单位
- School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, PR China.China
- 通讯作者单位
- School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, PR China. Electronic address: zhuff@sjtu.edu.cn.China
- 文献类型
- 综述
- 期刊
- Cancer letters2025 Aug 1
- 原文标识
- PubMed 40274063 · DOI 10.1016/j.canlet.2025.217737