ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Decoy Extracellular Vesicles Overcome Triple-Negative Breast Cancer Heterogeneity via Membrane-Cytoplasm-Mitochondria Cascade Targeting.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed.
- Mitochondria-Targeted Multimodal Nanotherapeutics Suppress Oxidized mtDNA-Driven Inflammation at the Source.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- The Multifaceted Role of Extracellular Vesicles in Triple Negative Breast Cancer.International journal of molecular sciences · 2026Review
- From Cold to Hot: Nanozyme-Based Strategies for Reprogramming the Tumour Immunoenvironment.Cell proliferation · 2026Review
- Global research trends and emerging frontiers of nanozymes in cancer therapy based on bibliometric and knowledge mapping analysis from 2001 to 2025.Discover nano · 2026Review
- Overcoming immunotherapy resistance in triple-negative breast cancer: a critical review of mast cell plasticity, metabolic reprogramming, and organoid models.Frontiers in immunology · 2026Review
- Recent advances of metal-organic frameworks (MOFs) for drug delivery, cancer imaging and theranostics.Theranostics · 2026Review
- The role of TEAD4 gene in the Hippo signaling pathway in triple-negative breast cancer and targeted therapy strategies.BMC medical genomics · 2025Article
- Decoy Extracellular Vesicles Overcome Triple-Negative Breast Cancer Heterogeneity via Membrane-Cytoplasm-Mitochondria Cascade Targeting.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Overcoming resistance to PD-1 and CTLA-4 blockade mechanisms and therapeutic strategies.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Triple-negative breast cancer (TNBC) exhibits multilevel heterogeneity, including differences in stemness, immune checkpoint (IC) upregulation, and metabolic plasticity, which has resulted in a lack, of comprehensive treatment strategies. Extracellular vesicles (EVs) from exhausted T cells contain high levels of ICs, which allow them to target and block multiple IC ligands in tumor cells, including cancer stem cells (CSCs). TEAD4 is identified as a pivotal gene facilitating CSC growth and immune escape. Consequently, a novel EV delivery system (siT/MOF@EVs), which targets the tumor cell membrane-cytoplasm-mitochondria cascade, is engineered to codeliver TEAD4-siRNA (siTEAD4) and a mitochondria-targeting metal-organic framework (T/MOF) to overcome tumor heterogeneity. Extracellularly, EVs act as "decoys" by facilitating the binding of IC ligands to target tumor cells, particularly CSCs, and blocking multiple ICs. Within the cytoplasm, the siTEAD4 adsorbed on the T/MOF surface is released, inhibiting CSCs and overcoming immunotherapy resistance. In mitochondria, cascade catalysis by nanozymes that bind monoatomic Pd and Mn
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.