氧化应激
纳米医学
活性氧
铜
氧化磷酸化
程序性细胞死亡
细胞生物学
线粒体
线粒体ROS
细胞
生物物理学
肿瘤微环境
癌细胞
细胞内
化学
细胞生长
铜毒性
细胞凋亡
线粒体毒性
细胞损伤
巨噬细胞
细胞培养
线粒体通透性转换孔
癌症研究
作者
Jun Tao,Weiqing Ning,Xuzhi Shi,Tingting Wu,Shenzhe Liu,Shuangshuang Wan,Shouju Wang,Jia Chen,Lianhui Wang
出处
期刊:ACS Nano
[American Chemical Society]
日期:2025-09-13
卷期号:19 (37): 33587-33600
被引量:2
标识
DOI:10.1021/acsnano.5c11565
摘要
Amplifying cellular oxidative stress damage is of great significance for triple-negative breast cancer (TNBC) treatment. However, high levels of mitochondrial copper metabolism effectively reverse oxidative damage and suppress TNBC apoptosis. Herein, we reported a copper depletion moiety (CDM) composed of a copper chelator and near-infrared heptamethine cyanine agent (IR780) for selective mitochondrial copper depletion and oxidative stress amplification. The as-prepared CDM could assemble with distearoyl phosphoethanolamine-PEG 2000 -COOH into self-delivery nanomedicine (CDM NPs) with improved hydrophilicity and excellent dispersion. Furthermore, compared to free CDM, these obtained CDM NPs display 9.26-fold, 1.16-fold, and 14.5-fold enhancement in cellular internalization, mitochondria targeting, and tumor accumulation, respectively. And they could efficiently induce mitochondrial copper depletion and burst production of reactive oxygen species under 808 nm laser irradiation, leading to powerful mitochondrial damage, oxidative stress imbalance, and upgraded immunogenic cell death. Apart from these, this synergistic mitochondrial copper depletion and oxidative stress elevation strategy significantly reverses the immunosuppressive microenvironment (promotes dendritic cell maturation and T cell vivification, regulates macrophage polarization and myeloid-derived suppressor cell infiltration), activates T cells in the spleen, and accelerates TNBC death with almost negligible systemic toxicity and is expected to provide perspective for the treatment of TNBC.
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