ArticleNature communications2023
Inhibition of glycolysis-driven immunosuppression with a nano-assembly enhances response to immune checkpoint blockade therapy in triple negative breast cancer.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 93 citations in OpenAlex.
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- Pollen-Based Artificial Enzyme With Efficient Biocatalysis and Immune-Priming to Prevent Primary and Secondary Wound Infection.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Protein Posttranslational Modifications in Immunity: Molecular Mechanisms and Therapeutic Targets.MedComm · 2026Review
- YTHDC1 Orchestrates Glucose and Glutamate Rewiring to Overcome Lethal Metabolic Stress in Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Strategies for Targeting Mitochondria in the Treatment of Breast Cancer.ACS pharmacology & translational science · 2026Review
- HAdvanced materials (Deerfield Beach, Fla.) · 2026Article
- IrMn-Cluster-Based Artificial Metalloenzymes with Radiosensitized Systemic Antitumor Responses to Prevent Malignant Tumor Metastasis and Recurrence.Nano-micro letters · 2026Article
- Cancer stem cell plasticity: mechanisms, immune microenvironment crosstalk, and therapeutic implications.Journal of hematology & oncology · 2026Review
- Article
- Research progress on precision targeted therapy strategies for breast cancer based on tumor microenvironment.iScience · 2026Review
- Regulatory T cells in cancer and inflammation.Signal transduction and targeted therapy · 2026Review
- Biomimetic nanomodulator reprograms glycolysis-driven immunosuppressive microenvironment to potentiate photothermal immunotherapy in cold tumors.Materials today. Bio · 2026Article
- Potentiated Tumor Photo-immunotherapy Based on Glutamine Starvation and Interferon Stimulatory DNA-Activated cGAS-STING Pathway.ACS medicinal chemistry letters · 2026Article
- Modeling VEGF and GLUT1 Expression as Coadapted Foraging Strategies in Cancer.bioRxiv : the preprint server for biology · 2026Article
- Targeting KIF20A blocks lactylation modification to suppress immune escape in hepatocellular carcinoma.iScience · 2026Article
- The Next Wave of Immunotherapy: A Critical Review of Nanotechnology Strategies for Immune Checkpoint Blockade.Pharmaceutics · 2026Review
- The fluoroquinoline compound exerts anti-erythroleukemic effects by dual-targeting GLUT1 and the PI3K/AKT signaling pathway.Scientific reports · 2026Article
- The emerging role of aptamers in targeted cancer immunotherapy.Molecular therapy. Oncology · 2026Review
- SLC2A1Nature cell biology · 2026Article
- Glucose-transporter 1 (GLUT1) as a prognostic biomarker: evidence from 14,966 human tumors across 134 cancer types.BMC cancer · 2026Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immune-checkpoint inhibitors (ICI) are promising modalities for treating triple negative breast cancer (TNBC). However, hyperglycolysis, a hallmark of TNBC cells, may drive tumor-intrinsic PD-L1 glycosylation and boost regulatory T cell function to impair ICI efficacy. Herein, we report a tumor microenvironment-activatable nanoassembly based on self-assembled aptamer-polymer conjugates for the targeted delivery of glucose transporter 1 inhibitor BAY-876 (DNA-PAE@BAY-876), which remodels the immunosuppressive TME to enhance ICI response. Poly β-amino ester (PAE)-modified PD-L1 and CTLA-4-antagonizing aptamers (aptPD-L1 and aptCTLA-4) are synthesized and co-assembled into supramolecular nanoassemblies for carrying BAY-876. The acidic tumor microenvironment causes PAE protonation and triggers nanoassembly dissociation to initiate BAY-876 and aptamer release. BAY-876 selectively inhibits TNBC glycolysis to deprive uridine diphosphate N-acetylglucosamine and downregulate PD-L1 N-linked glycosylation, thus facilitating PD-L1 recognition of aptPD-L1 to boost anti-PD-L1 therapy. Meanwhile, BAY-876 treatment also elevates glucose supply to tumor-residing regulatory T cells (Tregs) for metabolically rewiring them into an immunostimulatory state, thus cooperating with aptCTLA-4-mediated immune-checkpoint inhibition to abolish Treg-mediated immunosuppression. DNA-PAE@BAY-876 effectively reprograms the immunosuppressive microenvironment in preclinical models of TNBC in female mice and provides a distinct approach for TNBC immunotherapy in the clinics.
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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.