Repurposing flubendazole for glioblastoma ferroptosis by affecting xCT and TFRC proteins.

ABSTRACT: 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 <1‰), cell viability was inhibited in a concentration-dependent manner (IC₅₀ for LN229 = 0.5331 μM, IC₅₀ for U251 = 0.6809 μM), attributed to the induction of ferroptosis, as evidenced by increased MDA levels, accumulation of ROS and lipid peroxides, change in mitochondrial membrane potential and structure. Protein analysis related to ferroptosis showed upregulati

SUBMITTER: Teng W 

PROVIDER: S-EPMC11563996 | biostudies-literature | 2024 Nov

REPOSITORIES: biostudies-literature