ArticleNanoscale horizons2021
Tumor-targeted gene therapy with lipid nanoparticles inhibits tumor-associated adipocytes and remodels the immunosuppressive tumor microenvironment in triple-negative breast cancer.
Article in Nanoscale horizons, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 70 citations in OpenAlex.
- Cancer-associated adipocytes: metabolic reprogramming, crosstalk and therapeutic implications in tumor progression.Signal transduction and targeted therapy · 2026Review
- Targeting cytokine/chemokine signaling to convert immunologically cold tumors into hot: Emerging strategies in cancer immunotherapy.Acta pharmaceutica Sinica. B · 2026Review
- Immune Roles of Canonically Non-Immune Cells in Biomaterials Response.Cell biomaterials · 2026Article
- Metabolic crosstalk among cancer-associated fibroblasts, adipocytes and immune cells as an immunosuppressive tumor microenvironment driver.Experimental & molecular medicine · 2026Review
- Emerging Protein Targets in Triple-Negative Breast Cancer: Beyond Conventional Therapy.Cancers · 2026Review
- The progress and perspective of nanomedicine in modulating the tumor immune microenvironment.Acta pharmaceutica Sinica. B · 2026Review
- Cancer-associated adipocyte promote progression and immunosuppression in triple-negative breast cancer.Frontiers in oncology · 2026Article
- The chemokine network in triple-negative breast cancer: its role in immune microenvironment regulation, and prospects for targeted therapy.Frontiers in immunology · 2026Review
- Delivery of nucleic acid drugs for tumor therapy: Opportunities and challenges.Fundamental research · 2025Review
- Autophagy-Mediated Suppression of Tumor Growth by Food-Grade Lipid Nanoparticles in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Celastrol-loaded ginsenoside Rg3 liposomes boost immunotherapy by remodeling obesity-related immunosuppressive tumor microenvironment in melanoma.Acta pharmaceutica Sinica. B · 2025Article
- Chemokines as key mediators in RIPI: pathophysiology and translational potential.Frontiers in immunology · 2025Review
- Unveiling the impact of lipid metabolism on triple-negative breast cancer growth and treatment options.Frontiers in oncology · 2025Review
- Roles of tumor-associated macrophages in triple-negative breast cancer progression.Frontiers in immunology · 2025Review
- Shifting cold to hot tumors by nanoparticle-loaded drugs and products.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- Integrated analysis reveals prognostic correlation and immune characteristics of a tumor-associated macrophage-based risk signature in triple-negative breast cancer.Translational cancer research · 2024Article
- Dissecting the emerging role of cancer-associated adipocyte-derived cytokines in remodeling breast cancer progression.Heliyon · 2024Review
- Impact of obesity‑associated myeloid‑derived suppressor cells on cancer risk and progression (Review).International journal of oncology · 2024Review
- Advanced gene therapy system for the treatment of solid tumour: A review.Materials today. Bio · 2024Review
- Population-Specific gene expression profiles in prostate cancer: insights from Weighted Gene Co-expression Network Analysis (WGCNA).World journal of surgical oncology · 2024Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Adipocytes are the primary cellular components within the tumor microenvironment (TME) of triple-negative breast cancer (TNBC). Increasing evidence suggests that tumor-associated adipocytes (TAAs) can aggravate tumor progression, exacerbate the immunosuppressive TME and compromise therapeutic efficacy. In this study, the biological effect of TAAs within the breast cancer TME is first investigated, and the C-C Motif Chemokine Ligand 2 (CCL2) which is mainly secreted by TAAs in the extracellular environment is identified as the key mediator. CCL2 recruits immune cells such as monocytes and macrophages that further differentiated into immunosuppressive myeloid-derived suppressor cells (MDSCs) and M2 macrophages. To manipulate CCL2-mediated immune response, a protein trap that binds with CCL2 with high affinity and specificity is designed. The plasmid DNA encoding the CCL2 trap (pCCL2) is specifically delivered to the TME by using targeted lipid-protamine-DNA (LPD) nanoparticles to locally express the CCL2 trap and ameliorate the immunosuppressive TME. Significantly, compared with the commercially available CCL2 antibody, this strategy shows enhanced therapeutic efficacy and appreciable tumor growth inhibition. Furthermore, the pCCL2 trap treatment successfully suppresses TAAs, increases T cell infiltration and decreases the population of immunosuppressive M2 macrophages and MDSCs. Further studies show that the pCCL2 trap could facilitate PD-L1 blockade immunotherapy, demonstrating its translation potential.
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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.