粒体自噬
肿瘤微环境
免疫原性细胞死亡
免疫系统
癌症研究
癌细胞
细胞生物学
免疫检查点
癌症
线粒体
程序性细胞死亡
生物
材料科学
自噬
免疫疗法
细胞凋亡
免疫学
生物化学
遗传学
作者
Zhilong Wang,Qian Wang,Hongmei Cao,Zhongyan Wang,Dianyu Wang,Jinjian Liu,Tongxin Gao,Chunhua Ren,Jianfeng Liu
标识
DOI:10.1002/adma.202311043
摘要
Abstract The inherent immune and metabolic tumor microenvironment (TME) of most solid tumors adversely affect the antitumor efficacy of various treatments, which is an urgent issue to be solved in clinical cancer therapy. In this study, a mitochondrial localized in situ self‐assembly system is constructed to remodel the TME by improving immunogenicity and disrupting the metabolic plasticity of cancer cells. The peptide‐based drug delivery system can be pre‐assembled into nanomicelles in vitro and form functional nanofibers on mitochondria through a cascade‐responsive process involving reductive release, targeted enrichment, and in situ self‐assembly. The organelle‐specific in situ self‐assemblyeffectively switches the role of mitophagy from pro‐survival to pro‐death, which finally induces intense endoplasmic reticulum stress and atypical type II immunogenic cell death. Disintegration of the mitochondrial ultrastructure also impedes the metabolic plasticity of tumor cells, which greatly promotes the immunosuppresive TME remodeling into an immunostimulatory TME. Ultimately, the mitochondrial localized in situ self‐assembly system effectively suppresses tumor metastases, and converts cold tumors into hot tumors with enhanced sensitivity to radiotherapy and immune checkpoint blockade therapy. This study offers a universal strategy for spatiotemporally controlling supramolecular self‐assembly on sub‐organelles to determine cancer cell fate and enhance cancer therapy.
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