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:Role of tumor-derived exosomes mediated immune cell reprograming in cancer.
Role of tumor-derived exosomes mediated immune cell reprograming in cancer.
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肿瘤来源外泌体(TDEs)作为肿瘤细胞的拓扑结构,不仅携带母细胞的生物学信息,还充当细胞间通讯的信使。已有研究表明,TDEs在诱导免疫抑制性肿瘤微环境(TME)中发挥关键作用。它们可通过递送抑制性蛋白、细胞因子、RNA及其他物质,间接或直接地重编程免疫细胞。它们不仅抑制树突状细胞(DCs)和自然杀伤(NK)细胞的成熟与功能,还重塑M2巨噬细胞并抑制T细胞浸润,从而促进免疫抑制,为肿瘤生长、侵袭和转移创造有利的生态位。基于TDEs的特异性,靶向TDEs已成为监测肿瘤进展和增强治疗效果的新策略。本文综述了TDEs诱导免疫抑制效应所涉及的复杂分子机制,为癌症治疗奠定理论基础。此外,还讨论了TDEs作为肿瘤治疗新方法所面临的挑战。
Tumor-derived exosomes (TDEs), as topologies of tumor cells, not only carry biological information from the mother, but also act as messengers for cellular communication. It has been demonstrated that TDEs play a key role in inducing an immunosuppressive tumor microenvironment (TME). They can reprogram immune cells indirectly or directly by delivering inhibitory proteins, cytokines, RNA and other substances.
They not only inhibit the maturation and function of dendritic cells (DCs) and natural killer (NK) cells, but also remodel M2 macrophages and inhibit T cell infiltration to promote immunosuppression and create a favorable ecological niche for tumor growth, invasion and metastasis.
Based on the specificity of TDEs, targeting TDEs has become a new strategy to monitor tumor progression and enhance treatment efficacy. This paper reviews the intricate molecular mechanisms underlying the immunosuppressive effects induced by TDEs to establish a theoretical foundation for cancer therapy.
Additionally, the challenges of TDEs as a novel approach to tumor treatment are discussed.
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