ArticleJournal of nanobiotechnology2026
Biomimetic proteolipid vesicles delivering small activating RNA to activate the macrophage immunotherapy for the treatment of lung cancer.
Article in Journal of nanobiotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- MicroRNA regulation of macrophage polarization in lung cancer: Regulatory networks and therapeutic potential (Review).International journal of oncology · 2026Review
- Small Activating RNAs: A Curated Database and an Overview of Rational Design Principles.Molecules (Basel, Switzerland) · 2026Review
- In vivo CAR-M therapy: advancing precision delivery and programmable immune remodeling.Cell communication and signaling : CCS · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
Abstract
backgroundTumor-associated macrophages (TAMs) in the tumor microenvironment (TME) typically polarize toward an M2 phenotype that promotes tumor progression and immune suppression. Reprogramming TAMs to the proinflammatory M1 phenotype has emerged as a promising strategy to boost antitumor immunity. This study aimed to develop a targeted nanoplatform to deliver small activating RNAs (saRNAs) that upregulate genes involved in macrophage reprogramming.
resultsWe designed saRNAs targeting the promoters of p38 and TFEB, encapsulated within a metal-organic framework (MOF)-based delivery system and cloaked with hybrid membranes composed of synthetic lipids and exosome-derived vesicles. These were further functionalized with the TAM-targeting peptide CRV (CRVLRSGSC), resulting in nanoparticles termed CLMSR. CLMSR selectively accumulated in macrophages, enhancing intracellular saRNA delivery. Functional assays revealed that conditioned medium from CLMSR-treated M2 macrophages suppressed tumor cell migration, invasion, and 3D spheroid formation. In vivo, CLMSR demonstrated prolonged circulation time and enhanced tumor targeting. Importantly, treatment remodeled the TME by increasing CD8⁺ and CD4⁺ T cell infiltration and promoting TAM repolarization from the M2 to M1 phenotype.
conclusionsOur findings demonstrate that CLMSR represents a novel and efficient nanoplatform for saRNA delivery to reprogram TAMs and modulate the TME. By targeting M2 macrophages and inducing their transition to the tumoricidal M1 phenotype, this approach offers a promising therapeutic avenue to enhance antitumor immunity and inhibit tumor progression.
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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.