ArticleCell death discovery2026
Ferroptosis-induced oxidative stress in therapy-resistant glioblastoma.
Article in Cell death discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Authors and funding
14 authors.
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Abstract
Temozolomide (TMZ) resistance remains a major obstacle in glioma treatment. Ferroptosis, an iron-dependent, lipid peroxidation-driven regulated cell death, represents a promising alternative strategy. We investigated molecular determinants of ferroptosis sensitivity in TMZ-resistant glioma, focusing on HIF-1α and oxidative stress. One TMZ-sensitive (U251) and three TMZ-resistant (T98, U118, LN18) cell lines were treated with ferroptosis inducers (Erastin, FIN56, RSL3). Viability, ROS (total and mitochondrial), lipid peroxidation, and ferroptosis-related gene/protein expression were assessed. MitoTEMPO and deferoxamine (DFX) were used to probe mitochondrial ROS and iron dependence, respectively. Integrated metabolomic-proteomic analyses and an orthotopic U118-Luc model supported in vitro findings. Ferroptosis inducers reduced viability and bypassed TMZ resistance in vitro and suppressed tumor growth in vivo with partial body-weight loss. Resistant cells displayed high HIF-1α with elevated GSH/NRF2 activity and reduced lipid peroxidation. Treatments increased oxidative stress and downregulated GPX4, xCT, FSP1, and ATF4; MitoTEMPO rescued cells, implicating mitochondrial ROS. Ferroptosis induction reduced HIF-1α expression/nuclear localization and decreased HIF-1α/VEGF/SOX2/NRF2 in tumor tissue, supporting therapeutic potential.
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