ArticleInternational journal of molecular sciences2025
Polymeric Polylactic Acid-Glycolic Acid-Based Nanoparticles Deliver Nintedanib Across the Blood-Brain Barrier to Inhibit Glioblastoma Growth.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The trial behind it
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Who cites it
2 citing papers in PubMed.
- Redundancy in Growth Factor Receptor Signaling in Adult Astrocytoma Resistance to Small-Molecule Tyrosine Kinase Inhibitors.International journal of molecular sciences · 2026Review
- A Review of FDA-Approved Multi-Target Angiogenesis Drugs for Brain Tumor Therapy.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to investigate the inhibitory effect of nintedanib (BIBF) on glioblastoma (GBM) cells and its mechanism of action and to optimize a drug delivery strategy to overcome the limitations posed by the blood-brain barrier (BBB). We analyzed the inhibition of GBM cell lines following BIBF treatment and explored its effect on the autophagy pathway. The cytotoxicity of BIBF was assessed using the CCK-8 assay, and further techniques such as transmission electron microscopy, Western blotting (WB), and flow cytometry were employed to demonstrate that BIBF could block the autophagic pathway by inhibiting the fusion of autophagosomes and lysosomes, ultimately limiting the proliferation of GBM cells. Molecular docking and surface plasmon resonance (SPR) experiments indicated that BIBF specifically binds to the autophagy-associated protein VPS18, interfering with its function and inhibiting the normal progression of autophagy. However, the application of BIBF in GBM therapy is limited due to restricted drug penetration across the BBB. Therefore, this study utilized poly-lactic-co-glycolic acid (PLGA) nanocarriers as a drug delivery system to significantly enhance the delivery efficiency of BIBF in vivo. In vitro cellular experiments and in vivo animal model validation demonstrated that PLGA-BIBF NPs effectively overcame the limitations of the BBB, significantly enhanced the antitumor activity of BIBF, and improved therapeutic efficacy in a GBM BALB/c-Nude model. This study demonstrated that BIBF exerted significant inhibitory effects on GBM cells by binding to VPS18 and inhibiting the autophagy pathway. Combined with the PLGA nanocarrier delivery system, the blood-brain barrier permeability and anti-tumor effect of BIBF were significantly enhanced. Targeting the BIBF-VPS18 pathway and optimizing drug delivery through nanotechnology may represent a new strategy for GBM treatment, providing innovative clinical treatment ideas and a theoretical basis for patients with GBM.
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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.