化学
坏死性下垂
内质网
自噬
细胞生物学
活性氧
线粒体
生物物理学
程序性细胞死亡
黑色素瘤
癌细胞
未折叠蛋白反应
声动力疗法
氧化应激
缺氧(环境)
细胞凋亡
兰尼定受体
细胞
巨噬细胞
纳米医学
癌症研究
细胞毒性
一氧化氮
免疫原性细胞死亡
肿瘤缺氧
纳米技术
树突状细胞
作者
Xianbo Wu,Zeqi Li,Tiantian Yin,Jun Shu,Yin-Sui Xu,Jinzhe Liang,Xiting Zhang,Hui Chao
摘要
Hypoxic solid tumors present significant obstacles to cancer immunotherapy, primarily due to inadequate reactive oxygen species (ROS) production and profound immunosuppression. In this study, we rationally designed two Ir(III)-carbon nitride nanocomplexes, Ir 309 – C 3 N 5 and Ir 443 – C 3 N 5, fabricated using Ir(III) polypyridine complexes as precursors and C 3 N 5 nanosheets as nanoligands. Notably, benzothiazole modification of Ir 443 – C 3 N 5 imparted ultrasound-independent chemotherapeutic activity via ligand design, enabling the induction of oncosis even without ultrasound (US) stimulation. This modification simultaneously narrowed the bandgap, increased the dipole moment and piezoelectric coefficient, and stabilized metal-to-ligand charge transfer (MLCT) states, thereby extending charge-separated state lifetimes and enhancing ROS generation. Under US irradiation, Ir 443 – C 3 N 5 demonstrated superior self-sufficient oxygen supply and ROS production efficiency, leading to effective carrier utilization. Mechanistically, Ir 443 – C 3 N 5 @PEG selectively accumulated in mitochondria and the endoplasmic reticulum (ER), inducing ER stress and triggering oncosis, while US activation amplified oxidative stress to initiate necroptosis. The concurrent induction of oncosis and necroptosis fostered robust immunogenic cell death (ICD), dendritic cell maturation, macrophage polarization, and cytotoxic T-cell activation. As a result, this two-dimensional Ir(III)-based nanoplatform synergistically combines chemo- and sono-immunotherapy to overcome hypoxia and immunosuppression, effectively suppressing tumor metastasis and recurrence in melanoma-bearing mice.
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