ArticleJournal of nanobiotechnology2025
Sono-triggered endoplasmic reticulum-targeted ROS burst silencing CD300ld to alleviate polymorphonuclear myeloid-derived suppressor cells for breast cancer treatment.
Article in Journal of nanobiotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
1 citing paper in PubMed.
- CD300ld blockade overcomes PMN-MDSC-mediated vaccine resistance in advanced tumors.Journal for immunotherapy of cancer · 2026Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Immunogenic cell death (ICD) significantly boosts anti-tumor immunotherapy effectiveness; however, the recruitment of polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs), driven by factors such as adenosine accumulation and oxygen depletion during ICD, impairs the overall therapeutic outcome as well as facilitates tumor development and metastasis. Recent studies identify CD300ld as a key regulator of PMN-MDSCs recruitment, making it a promising immunotherapeutic target. Here, an innovative strategy is developed to eminently amplify ICD while alleviating PMN-MDSC infiltration upon ultrasound (US) stimulation. A modified generation 5 (G5) poly(amidoamine) dendrimer (G5PBA) was employed to encapsulate hematoporphyrin (GH)-a widely used organic sonosensitizer-and modified the complex with pardaxin peptides (Par) to achieve precise endoplasmic reticulum (ER) targeting, and adsorbed the negatively charged siCD300ld (PGH@siRNA). Under US irradiation, PGH@siRNA precisely accumulates at ER to induce localized reactive oxygen species (ROS) bursts, and effectively silence CD300ld, thereby amplifying endoplasmic reticulum stress (ERS)-mediated ICD and reducing PMN-MDSCs infiltration to reshape the tumor microenvironment. This systematic preclinical evaluations demonstrated enhanced immune activation, suppressed metastasis, and improved therapeutic outcomes. This study introduces a sono-responsive synergistic strategy integrating ER-targeted sonodynamic therapy with gene silencing, offering a novel paradigm for targeting PMN-MDSCs and enhancing triple-negative breast cancer (TNBC) immunotherapy.
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Registered trials
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