ArticleBritish journal of pharmacology2020
A low MW inhibitor of CD44 dimerization for the treatment of glioblastoma.
Article in British journal of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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
24 citing papers in PubMed, 35 citations in OpenAlex.
- Targeting CD44 reverses sphingomyelin-induced oligodendrocyte maturation arrest in acid sphingomyelinase deficiency.EMBO molecular medicine · 2026Article
- CD44 antagonism after traumatic brain injury influences the adult neurogenic niche and behavioral outcomes.Brain structure & function · 2026Article
- Natural polysaccharides as multifunctional anti-cancer agents: structure-activity relationships, mechanisms of action, and therapeutic potential.Frontiers in immunology · 2026Review
- Antioxidants Acteoside and Orientin as Emerging Agents in Synergistic Cancer Therapy: A Focus on Innovative Applications.Antioxidants (Basel, Switzerland) · 2025Review
- Killing the killers: Natural killer cell therapy targeting glioma stem cells in high-grade glioma.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Revisiting Treatment Strategies: Addressing Epithelial-to-Mesenchymal Transition-Induced Resistance in Hepatocellular Carcinoma.BME frontiers · 2025Review
- The cell adhesion molecule CD44 acts as a modulator of 5-HT7 receptor functions.Cell communication and signaling : CCS · 2024Article
- CD44 and its implication in neoplastic diseases.MedComm · 2024Review
- Informed by Cancer Stem Cells of Solid Tumors: Advances in Treatments Targeting Tumor-Promoting Factors and Pathways.International journal of molecular sciences · 2024Review
- Osteopontin-driven partial epithelial-mesenchymal transition governs the development of middle ear cholesteatoma.Cell cycle (Georgetown, Tex.) · 2024Article
- Review
- The Bone Marrow Immune Microenvironment in CML: Treatment Responses, Treatment-Free Remission, and Therapeutic Vulnerabilities.Current hematologic malignancy reports · 2023Review
- Regulation of epithelial-mesenchymal transition by tumor microenvironmental signals and its implication in cancer therapeutics.Seminars in cancer biology · 2023Review
- Astrocyte 3D culture and bioprinting using peptide functionalized hyaluronan hydrogels.Science and technology of advanced materials · 2023Article
- Molecular mechanism of CD44 homodimerization modulated by palmitoylation and membrane environments.Biophysical journal · 2022Article
- Proteomics-based investigation of cerebrovascular molecular mechanisms in cerebral amyloid angiopathy by the FFPE-LMD-PCT-SWATH method.Fluids and barriers of the CNS · 2022Article
- Disruption of the pentraxin 3/CD44 interaction as an efficient therapy for triple-negative breast cancers.Clinical and translational medicine · 2022Article
- Novel Antibody Exerts Antitumor Effect through Downregulation of CD147 and Activation of Multiple Stress Signals.Journal of oncology · 2022Article
- The complex interactions between the cellular and non-cellular components of the brain tumor microenvironmental landscape and their therapeutic implications.Frontiers in oncology · 2022Review
- Macrophage-stroma interactions in fibrosis: biochemical, biophysical, and cellular perspectives.The Journal of pathology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
background and purposeAs a hallmark of glioblastoma multiforme (GBM), CD44 plays a crucial role in promoting glioblastoma stem cell (GSC) stemness phenotypes and multiple drug resistance. The therapeutic potential of CD44 has been validated by the clinical successes of several CD44 inhibitors, including antibodies and hyaluronan-related drugs. EXPERIMENTAL APPROACH: We used systemsDock software to predict verbascoside as a candidate CD44 inhibitor. Microscale thermophoresis was used to confirm the interaction between CD44 and verbascoside. Four glioblastoma cell lines and a patient-derived glioblastoma cell line were used to test the influences of verbascoside on glioblastoma. CD44-overexpressing and CD44-knockout cell lines were also used. Real-time quantitative PCR and western blot analyses were performed. A xenograft mouse model was used to test verbascoside. KEY
resultsVerbascoside bound to CD44 and suppressed its dimerization. By inhibiting CD44 dimerization, verbascoside decreased the release of the CD44 intracellular domain (CD44ICD) and suppressed the expression of CD44 downstream genes. Verbascoside treatment suppressed the stemness phenotypes of cells with high CD44 expression. In a mouse model of glioma, verbascoside treatment highly reduced the growth of intracranial tumours and inhibited CD44ICD release. Both stem cell marker and mesenchymal GBM subtype marker genes were down-regulated in verbascoside-treated mice. CONCLUSION AND IMPLICATIONS: Verbascoside suppressed growth of glioblastoma cells by inhibiting CD44 dimerization. Stem cell-like cell properties and tumour cell growth were also suppressed by verbascoside, both in vitro and in vivo. Verbascoside significantly prolonged survival of xenografted mice.
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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.