ArticleBiomaterials research2023
Inhibition of DAMP actions in the tumoral microenvironment using lactoferrin-glycyrrhizin conjugate for glioblastoma therapy.
Article in Biomaterials research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Lactoferrin and Nanotechnology: New Insights Into Glioblastoma Therapy.CNS neuroscience & therapeutics · 2026Review
- BBB-aware stimuli-responsive and biomimetic nanomedicines for glioblastoma.Chinese neurosurgical journal · 2026Review
- Review
- Neutrophil Extracellular Traps in Cancer Metastasis: From Mechanistic Understanding to Targeted Therapy.Current oncology (Toronto, Ont.) · 2026Review
- Glycyrrhizic acid-loaded biomimetic hybrid liposomes targeting inflammatory cascades and PD-1/PD-L1 pathway to reverse neuroinflammation-driven cognitive decline.Materials today. Bio · 2026Article
- Advances in Drug Delivery Systems Utilizing Glycyrrhizic Acid and Its Aglycone Glycyrrhetinic Acid in Cancer Therapy.International journal of nanomedicine · 2026Review
- Construction and In Vitro Evaluation of Brain-Targeted Lutein Liposomes.Foods (Basel, Switzerland) · 2025Article
- Glycyrrhizin mediates autophagy through the STAT3/survivin pathway to inhibit proliferation and angiogenesis in hepatoma cells.Cytotechnology · 2025Article
- Recent advances in nanomaterial-based brain-targeted delivery systems for glioblastoma therapy.Nanomedicine (London, England) · 2025Review
- Nano-reduction of whey protein using ultra-sonication as a novel approach to improve its applicability in food industry.Ultrasonics sonochemistry · 2025Article
- Molecular Subtyping and Therapeutic Targeting of IFNG-Driven Immunogenic Cell Death in Lung Adenocarcinoma.Cancer medicine · 2025Article
- Smart delivery vehicles for cancer: categories, unique roles and therapeutic strategies.Nanoscale advances · 2024Review
- An update on pathogenesis and clinical scenario for Parkinson's disease: diagnosis and treatment.3 Biotech · 2023Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundHigh-mobility group box-1 (HMGB1) released from the tumor microenvironment plays a pivotal role in the tumor progression. HMGB1 serves as a damaged-associated molecular pattern (DAMP) that induces tumor angiogenesis and its development. Glycyrrhizin (GL) is an effective intracellular antagonist of tumor released HMGB1, but its pharmacokinetics (PK) and delivery to tumor site is deficient. To address this shortcoming, we developed lactoferrin-glycyrrhizin (Lf-GL) conjugate.
methodsBiomolecular interaction between Lf-GL and HMGB1 was evaluated by surface plasmon resonance (SPR) binding affinity assay. Inhibition of tumor angiogenesis and development by Lf-GL attenuating HMGB1 action in the tumor microenvironment was comprehensively evaluated through in vitro, ex vivo, and in vivo. Pharmacokinetic study and anti-tumor effects of Lf-GL were investigated in orthotopic glioblastoma mice model.
resultsLf-GL interacts with lactoferrin receptor (LfR) expressed on BBB and GBM, therefore, efficiently inhibits HMGB1 in both the cytoplasmic and extracellular regions of tumors. Regarding the tumor microenvironment, Lf-GL inhibits angiogenesis and tumor growth by blocking HMGB1 released from necrotic tumors and preventing recruitment of vascular endothelial cells. In addition, Lf-GL improved the PK properties of GL approximately tenfold in the GBM mouse model and reduced tumor growth by 32%. Concurrently, various biomarkers for tumor were radically diminished.
conclusionCollectively, our study demonstrates a close association between HMGB1 and tumor progression, suggesting Lf-GL as a potential strategy for coping with DAMP-related tumor microenvironment. HMGB1 is a tumor-promoting DAMP in the tumor microenvironment. The high binding capability of Lf-GL to HMGB1 inhibits tumor progression cascade such as tumor angiogenesis, development, and metastasis. Lf-GL targets GBM through interaction with LfR and allows to arrest HMGB1 released from the tumor microenvironment. Therefore, Lf-GL can be a GBM treatment by modulating HMGB1 activity.
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