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:NK-derived exosomes in anti-tumor strategies.
NK-derived exosomes in anti-tumor strategies.
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肿瘤仍然是当今研究人员面临的重大挑战之一。肿瘤的发生发展由遗传因素、环境暴露和稳态破坏驱动,导致正常细胞转化为恶性细胞。自然杀伤(NK)细胞是免疫治疗中一类关键的免疫细胞,无需肿瘤抗原预先刺激即可直接识别并清除肿瘤细胞。NK细胞来源的外泌体通过多种机制发挥抗肿瘤作用,包括释放细胞毒性分子、死亡受体配体介导的凋亡以及分泌细胞因子和其他生物活性分子。然而,未修饰外泌体的治疗效果受到活性成分不足、肿瘤微环境抑制以及缺乏靶向特异性的限制。载药和工程化策略可增强其治疗潜力。在本综述中,我们探讨了基于NK细胞来源外泌体(NK-Exos)的抗肿瘤策略的进展,重点关注涉及天然外泌体、载药外泌体和表面修饰外泌体用于清除肿瘤的研究。
Tumors remain one of the major challenges confronting researchers today. The development of tumor is driven by genetic factors, environmental exposures, and homeostatic disruptions, leading to the transformation of normal cells into malignant ones.
Natural killer (NK) cells, a crucial class of immune cells in immunotherapy, can directly recognize and eliminate tumor cells without prior stimulation by tumor antigens. Exosomes derived from NK cells exert anti-tumor effects through multiple mechanisms, including the release of cytotoxic molecules, death receptor ligand-mediated apoptosis, and the secretion of cytokines and other bioactive molecules.
However, the therapeutic efficacy of unmodified exosomes is constrained by insufficient active components, suppression by the tumor microenvironment, and a lack of targeting specificity. Drug loading and engineering strategies can enhance their therapeutic potential. In this review, we examine advancements in NK cell-derived exosome (NK-Exos)-based anti-tumor strategies, focusing on studies involving native exosomes, drug-loaded exosomes, and surface-modified exosomes for tumor eradication.
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