State Key Laboratory of Bioelectronics, Jiangsu Key Laboratory for Biomaterials and Devices, School of Biological Sciences and Medical Engineering, Southeast University, Nanjing, 210096, P. R. China.
Adv Sci (Weinh). 2023 Jun;10(18):e2300679. doi: 10.1002/advs.202300679. Epub 2023 Apr 21.
Universal chemotherapy in glioblastoma patients causes chemoresistance and further limits immune cells by creating an immunosuppressive tumor microenvironment that are difficult to solve by single-drug therapeutic approaches. Here, this work designs hybrid drug-loaded nanoliposomes by co-loading the chemotherapeutic drug temozolomide (TMZ) and nitric oxide (NO) prodrug JS-K with sphingosine-1-phosphate molecules (S1P) on the surface. The S1P-S1P receptors axis endows nanoliposomes with rapid targeting and lysosomal escaping capability. Then, fine-tuned TMZ release and NO gas production following JS-K release in glioma microenvironment decrease chemoresistance and increase tumor immunogenicity through inhibiting the cellular autophagy as well as inducing mitochondrial dysfunction. RNA sequencing analysis demonstrates that the NO gas generation reprograms glioma microenvironment immune and inflammation-related pathways. The positive immune response in turn effectively activates the enhanced efficacy of chemotherapy. NO gas generated nanoliposomes thus have attractive paradigm-shifting applications in the treatment of "cold" tumors across a range of immunosuppressive indications.
胶质母细胞瘤患者的通用化疗会导致化疗耐药性,并通过创建免疫抑制性肿瘤微环境进一步限制免疫细胞,而单一药物治疗方法很难解决这些问题。在这里,这项工作通过在表面上共载化疗药物替莫唑胺(TMZ)和一氧化氮(NO)前体 JS-K 以及神经鞘氨醇-1-磷酸分子(S1P)来设计混合载药纳米脂质体。S1P-S1P 受体轴赋予纳米脂质体快速靶向和溶酶体逃逸能力。然后,在胶质瘤微环境中精细调节 TMZ 的释放和 JS-K 释放后的 NO 气体生成,通过抑制细胞自噬和诱导线粒体功能障碍,降低化疗耐药性并增加肿瘤免疫原性。RNA 测序分析表明,NO 气体生成重编程了胶质瘤微环境免疫和炎症相关途径。正向免疫反应反过来又能有效地增强化疗的效果。因此,生成 NO 气体的纳米脂质体在治疗一系列免疫抑制性适应症的“冷”肿瘤方面具有吸引力的范式转变应用。