肿瘤细胞治疗研究
英文原题：NK cell vesicles-based nanoplatform loaded with sorafenib synergizing ferroptosis and antitumor immunity against hepatocellular carcinoma.
本研究提出了一种针对肝细胞癌（HCC）的新型治疗策略，通过协同诱导铁死亡并激活抗肿瘤免疫发挥作用，从而为 HCC 治疗开辟了新途径。
背景：铁死亡是一种依赖铁的细胞死亡形式，其特征为细胞内铁过量及脂质过氧化物积累。这一过程为癌症治疗提供了一种新颖且有前景的策略。增强铁死亡有望有效缓解常规治疗方法的局限。 方法：我们构建了一种协同纳米治疗平台。采用挤出法制备自然杀伤（NK）细胞来源纳米囊泡（NK-NV），随后通过电穿孔装载索拉非尼（SRB），制成用于靶向递送的NK-NV-SRB复合物。 结果：该治疗策略可逃避药物外排泵识别，从而减少药物外排，并有效诱导癌细胞发生铁死亡。这一过程显著释放损伤相关分子模式（DAMP），最终导致免疫原性细胞死亡（ICD）。体内实验显示，NK-NV-SRB干预的肿瘤生长抑制率为44.54%，可有效推动铁死亡进程，并通过募集CD8+ T细胞浸润激活抗肿瘤免疫。 结论：本研究提出了一种治疗肝细胞癌（HCC）的新策略，通过协同诱导铁死亡并激活抗肿瘤免疫发挥作用，为HCC治疗开辟了新途径。
BACKGROUND: Ferroptosis is a type of cell death that relies on iron and is marked by an excess of intracellular iron and the buildup of lipid peroxides. This process presents a new and promising approach for cancer treatment. Improving ferroptosis can effectively mitigate the limitations of conventional treatment methods. METHODS: We developed a synergistic nanotherapeutic platform. Natural killer cell derived nanovesicles (NK-NVs) were fabricated using an extrusion method and subsequently loaded with sorafenib (SRB) via electroporation, resulting in the NK-NVs-SRB complex for targeted delivery. RESULTS: The therapeutic strategy not only escaped recognition by drug efflux pumps, thus lowering drug expulsion, but also effectively triggered ferroptosis in cancer cells. This process induced significant release of damage associated molecular patterns (DAMPs), ultimately leading to immunogenic cell death (ICD). In vivo experiments demonstrated that NK-NVs-SRB intervention achieved a tumor growth inhibition rate of 44.54%, effectively drove the ferroptosis process, and activated anti-tumor immunity by recruiting CD8 + T cell infiltration. CONCLUSIONS: This study proposes a novel therapeutic strategy for hepatocellular carcinoma (HCC) that acts by synergistically inducing ferroptosis and activating anti-tumor immunity, thereby paving a new avenue for HCC treatment.
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