ArticleProceedings of the National Academy of Sciences of the United States of America2020
Lumefantrine, an antimalarial drug, reverses radiation and temozolomide resistance in glioblastoma.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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.
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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
25 citing papers in PubMed, 48 citations in OpenAlex.
- Effective approaches in conquering chemoresistance of glioblastoma: potential for nanoformulations.Drug delivery and translational research · 2026Review
- MicroRNA strand ratio disarray promotes temozolomide resistance in glioblastoma.Cellular & molecular biology letters · 2025Article
- Review
- Moesin silencing enhances the radiosensitivity of glioblastoma by inhibiting DNA damage repair via CD44/AKT1 signaling pathway.Discover oncology · 2025Article
- Role of Transcription Factor Fli-1 in Inflammation and Autoimmune Diseases.Biomolecules · 2025Review
- Lumefantrine ameliorates DSS-induced colitis by targeting FLI-1 to suppress NF-κB signaling.Frontiers in pharmacology · 2025Article
- FLI-1-driven regulation of endothelial cells in human diseases.Journal of translational medicine · 2024Review
- Overcoming Resistance to Temozolomide in Glioblastoma: A Scoping Review of Preclinical and Clinical Data.Life (Basel, Switzerland) · 2024Article
- RPL22L1, a novel candidate oncogene promotes temozolomide resistance by activating STAT3 in glioblastoma.Cell death & disease · 2023Article
- Mechanistic insights into super-enhancer-driven genes as prognostic signatures in patients with glioblastoma.Journal of cancer research and clinical oncology · 2023Article
- Review
- Targeting Heat Shock Proteins in Malignant Brain Tumors: From Basic Research to Clinical Trials.Cancers · 2022Review
- Drug Repurposing, a Fast-Track Approach to Develop Effective Treatments for Glioblastoma.Cancers · 2022Review
- Current insights into the role of Fli-1 in hematopoiesis and malignant transformation.Cellular and molecular life sciences : CMLS · 2022Review
- Wnt and PI3K/Akt/mTOR Survival Pathways as Therapeutic Targets in Glioblastoma.International journal of molecular sciences · 2022Review
- Identification of EMT-Related Genes and Prognostic Signature With Significant Implications on Biological Properties and Oncology Treatment of Lower Grade Gliomas.Frontiers in cell and developmental biology · 2022Article
- Article
- 5-Methylcytosine Related LncRNAs Reveal Immune Characteristics, Predict Prognosis and Oncology Treatment Outcome in Lower-Grade Gliomas.Frontiers in immunology · 2022Article
- The role of RNA modification in the generation of acquired drug resistance in glioma.Frontiers in genetics · 2022Review
- Comprehensive Analyses of Ferroptosis-Related Alterations and Their Prognostic Significance in Glioblastoma.Frontiers in molecular biosciences · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma multiforme (GBM) is an aggressive cancer without currently effective therapies. Radiation and temozolomide (radio/TMZ) resistance are major contributors to cancer recurrence and failed GBM therapy. Heat shock proteins (HSPs), through regulation of extracellular matrix (ECM) remodeling and epithelial mesenchymal transition (EMT), provide mechanistic pathways contributing to the development of GBM and radio/TMZ-resistant GBM. The Friend leukemia integration 1 (Fli-1) signaling network has been implicated in oncogenesis in GBM, making it an appealing target for advancing novel therapeutics. Fli-1 is linked to oncogenic transformation with up-regulation in radio/TMZ-resistant GBM, transcriptionally regulating HSPB1. This link led us to search for targeted molecules that inhibit Fli-1. Expression screening for Fli-1 inhibitors identified lumefantrine, an antimalarial drug, as a probable Fli-1 inhibitor. Docking and isothermal calorimetry titration confirmed interaction between lumefantrine and Fli-1. Lumefantrine promoted growth suppression and apoptosis in vitro in parental and radio/TMZ-resistant GBM and inhibited tumor growth without toxicity in vivo in U87MG GBM and radio/TMZ-resistant GBM orthotopic tumor models. These data reveal that lumefantrine, an FDA-approved drug, represents a potential GBM therapeutic that functions through inhibition of the Fli-1/HSPB1/EMT/ECM remodeling protein networks.
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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.