RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:Exosome-Mediated Crosstalk Between Cancer Cells and Tumor Microenvironment.
Exosome-Mediated Crosstalk Between Cancer Cells and Tumor Microenvironment.
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外泌体是细胞外囊泡,在介导肿瘤微环境(TME)内的细胞间通讯中发挥核心作用。肿瘤来源的外泌体携带蛋白质、核酸和脂质,重塑周围基质细胞和免疫细胞的表型与功能,从而促进肿瘤进展、血管生成、转移和治疗耐药。与此同时,来源于TME组分的外泌体,包括巨噬细胞、树突状细胞、B细胞、T细胞、成纤维细胞、中性粒细胞和NK细胞,反过来影响肿瘤生长和免疫逃逸。这些双向相互作用凸显了外泌体既是肿瘤进展的驱动因素,也是抗肿瘤免疫的调节因子。在本综述中,我们综合了当前关于外泌体重编程免疫细胞和基质细胞的多种机制的证据,重点关注其在癌症生物学中的双重作用。我们还讨论了抑制外泌体生物发生、释放和功能的新兴治疗策略,强调其作为癌症诊断和治疗新靶点的转化潜力。
Exosomes are extracellular vesicles that play a central role in mediating intercellular communication within the tumor microenvironment (TME). Cancer-derived exosomes carry proteins, nucleic acids, and lipids that reshape the phenotype and function of surrounding stromal and immune cells, thereby promoting tumor progression, angiogenesis, metastasis, and resistance to therapy.
At the same time, exosomes derived from TME components, including macrophages, dendritic cells, B cells, T cells, fibroblasts, neutrophils, and NK cells, reciprocally influence tumor growth and immune evasion. These bidirectional interactions highlight exosomes as both drivers of tumor progression and regulators of antitumor immunity. In this review, we synthesize current evidence on the diverse mechanisms by which exosomes reprogram immune and stromal cells, with a focus on their dual roles in cancer biology.
We also discuss emerging therapeutic strategies to inhibit exosome biogenesis, release, and function, underscoring their translational potential as novel targets for cancer diagnosis and treatment.
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