Repurposing flubendazole for glioblastoma ferroptosis by affecting xCT and TFRC proteins

New uses of old drugs hold great promise for clinical translation. Flubendazole, an FDA‐approved antiparasitic drug, has been shown to target p53 and promote apoptosis in glioblastoma (GBM) cells. However, its damaging mechanism in GBM remains elusive. Herein, we explored the ferroptosis‐inducing ab...

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Bibliographic Details
Published in:Journal of cellular and molecular medicine 2024-11, Vol.28 (22), p.e70188-n/a
Main Authors: Teng, Wei, Ling, Yuanguo, Long, Niya, Cen, Wu, Zhang, Hongzhi, Jiang, Lishi, Liu, Jian, Zhou, Xingwang, Chu, Liangzhao
Format: Article
Language:English
Subjects:
Amino Acid Transport System y+ - genetics
Amino Acid Transport System y+ - metabolism
Antiparasitic agents
Apoptosis
Apoptosis - drug effects
Brain Neoplasms - drug therapy
Brain Neoplasms - metabolism
Brain Neoplasms - pathology
Cell culture
Cell cycle
Cell death
Cell Line, Tumor
Cell lines
Cell Survival - drug effects
Cell viability
Clinical trials
Divalent metal transporter-1
Drug Repositioning
Ferroptosis
Ferroptosis - drug effects
Flow cytometry
Fubendazole
Gene Expression Regulation, Neoplastic - drug effects
Glioblastoma
Glioblastoma - drug therapy
Glioblastoma - metabolism
Glioblastoma - pathology
glioblastoma stem cell
Glioma
Glioma cells
Humans
Lipid peroxidation
Lipids
Mebendazole - analogs & derivatives
Mebendazole - pharmacology
Membrane potential
Membrane Potential, Mitochondrial - drug effects
Membranes
Molecular Docking Simulation
Morphology
Original
Oxidation
p53 Protein
Polyclonal antibodies
Protein structure
Proteins
Reactive Oxygen Species - metabolism
Receptors, Transferrin - metabolism
Software
Stem cells
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Description
Summary:New uses of old drugs hold great promise for clinical translation. Flubendazole, an FDA‐approved antiparasitic drug, has been shown to target p53 and promote apoptosis in glioblastoma (GBM) cells. However, its damaging mechanism in GBM remains elusive. Herein, we explored the ferroptosis‐inducing ability of flubendazole on GBM cells. After treating glioma cell lines U251 and LN229 with the flubendazole (DMSO
ISSN:1582-1838
1582-4934
1582-4934
DOI:10.1111/jcmm.70188