肿瘤微环境
免疫系统
效应器
癌症研究
免疫疗法
化学
氧化磷酸化
癌细胞
癌症免疫疗法
糖酵解
细胞毒性T细胞
厌氧糖酵解
细胞生物学
胶束
T细胞
癌相关成纤维细胞
生物
炎症
癌症
先天免疫系统
新陈代谢
PI3K/AKT/mTOR通路
免疫
乳腺肿瘤
肿瘤进展
细胞
免疫检查点
免疫原性细胞死亡
作者
Siyu Meng,Xuan Wei,Zhili Wang,Siyu Chen,Keying Chen,Jiamin Cheng,Z Chen,Jiabao Liang,Liangliang Dai
摘要
ABSTRACT Reversing the immunosuppressive tumor microenvironment by targeting metabolic competition between tumors and immune effector cells could induce tumor starvation and enhance the activity of immune cells, representing a potential approach to boost tumor immunotherapy. However, its actual efficacy is limited by compensatory oxidative phosphorylation (OXPHOS) energy replenishment and low delivery efficiency. Herein, we report a hydrogen sulfide (H 2 S)‐self‐supplying nanoplatform that orchestrates a dual blockade of glycolysis and OXPHOS for improved triple‐negative breast cancer (TNBC) immunotherapy. The micellar system, HA‐ADT@W, achieves tumor‐targeted delivery of a glycolysis inhibitor (WZB117) and H 2 S continually released in GSH‐overexpressed tumor cells. This strategy concurrently suppresses glucose uptake in tumor cells by reversing the acidic tumor microenvironment (TME) and disrupts compensatory OXPHOS via H 2 S‐mediated inhibition of cytochrome c oxidase. Consequently, we demonstrate a significant rewiring of tumor energy metabolism that not only induces immunogenic cell death with remodeling of the immunosuppressive TME but also alleviates nutrient constraints of immune effector cells, leading to enhanced infiltration and function of cytotoxic immune cells. This work exhibits a smart nanoplatform‐based H 2 S self‐supplied micelle for reinforced TNBC immunotherapy via regulated metabolic competition between tumors and immune effector cells with TME normalization.
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