ArticleInternational journal of molecular sciences2024
Mechanisms of Cell Death Induced by Erastin in Human Ovarian Tumor Cells.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Ferroptosis Suppressor Protein 1 (FSP1)-CoQ10-NADPH-Axis Is Responsible for Erastin Resistance in MCF-7 Breast Cancer Cells.Antioxidants (Basel, Switzerland) · 2026Article
- Metabolic cell deaths in head and neck cancer: mechanisms, therapeutic potential, and challenges.Annals of medicine · 2025Review
- Causal effects of ferroptosis-related traits on ovarian dysfunction: insights from integrating genome-wide Mendelian randomization, DNA methylation, gene expression, and proteome.Journal of ovarian research · 2025Article
- Ferroptosis in Toxicology: Present and Future.International journal of molecular sciences · 2025Review
- Ferroptosis in Cancer: Mechanism and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Ferroptosis Inducers Erastin and RSL3 Enhance Adriamycin and Topotecan Sensitivity in ABCB1/ABCG2-Expressing Tumor Cells.International journal of molecular sciences · 2025Article
- Targeting ferroptosis: a promising avenue for ovarian cancer treatment.Frontiers in immunology · 2025Review
- Targeting regulated cell death pathways in cancers for effective treatment: a comprehensive review.Frontiers in cell and developmental biology · 2024Review
- Metabolic consequences of erastin-induced ferroptosis in human ovarian cancer cells: an untargeted metabolomics study.Frontiers in molecular biosciences · 2024Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Erastin (ER) induces cell death through the formation of reactive oxygen species (ROS), resulting in ferroptosis. Ferroptosis is characterized by an accumulation of ROS within the cell, leading to an iron-dependent oxidative damage-mediated cell death. ER-induced ferroptosis may have potential as an alternative for ovarian cancers that have become resistant due to the presence of Ras mutation or multi-drug resistance1 (MDR1) gene expression. We used K-Ras mutant human ovarian tumor OVCAR-8 and NCI/ADR-RES, P-glycoprotein-expressing cells, to study the mechanisms of ER-induced cell death. We used these cell lines as NCI/ADR-RES cells also overexpresses superoxide dismutase, catalase, glutathione peroxidase, and transferase compared to OVCAR-8 cells, leading to the detoxification of reactive oxygen species. We found that ER was similarly cytotoxic to both cells. Ferrostatin, an inhibitor of ferroptosis, reduced ER cytotoxicity. In contrast, RSL3 (RAS-Selective Ligand3), an inducer of ferroptosis, markedly enhanced ER cytotoxicity in both cells. More ROS was detected in OVCAR-8 cells than NCI/ADR-RES cells, causing more malondialdehyde (MDA) formation in OVCAR-8 cells than in NCI/ADR-RES cells. RSL3, which was more cytotoxic to NCI/ADR-RES cells, significantly enhanced MDA formation in both cells, suggesting that glutathione peroxidase 4 (
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Registered trials
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