ArticleInternational journal of nanomedicine2025
Engineered
Article in International journal of nanomedicine, 2025. 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Engineered live bacteria for liver diseases and gut-liver axis disorders: from genetic modification to advanced delivery systems.Journal of nanobiotechnology · 2026Review
- Advancements on the synergistic application of oncolytic viruses and molecularly targeted therapies for the treatment of solid tumors (Review).International journal of oncology · 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
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Glypican-3 (GPC3), which is a membrane-associated antigen that is overexpressed in hepatocellular carcinoma (HCC). hGC33, a humanized anti-GPC3 antibody, has been validated as a potential antibody drug with good antitumor activity by preclinical studies and the Phase II clinical trial. However, free drug usually lack good tumor penetration. Outer membrane vesicles (OMVs) that are secreted by Methods: In this study, we utilized Results: hGC33-OMVs exhibited spherical bilayered nanostructures and displayed hGC33-scFv on their surface. hGC33-OMVs preferentially accumulated in tumors, significantly reducing tumor volume compared with controls and downregulating the proliferation markers Ki67 and PCNA. Transwell assays revealed increased tropism of hGC33-OMVs toward HepG2 cells, while Co-IP confirmed the direct interaction between hGC33 and GPC3. Meanwhile, hGC33-OMVs suppressed HepG2 cell proliferation, induced G1-phase arrest, and reduced Wnt3a, β-catenin, Cyclin D1, and C-myc expression. Conclusion: Engineered
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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.