ArticleFrontiers in oncology2020
Role of GPX4-Mediated Ferroptosis in the Sensitivity of Triple Negative Breast Cancer Cells to Gefitinib.
Article in Frontiers in oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 3 of them syntheses that pooled it.
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Who cites it
93 citing papers in PubMed, 3 syntheses or guidelines pooled it, 149 citations in OpenAlex.
- Targeting Ferroptosis as the Achilles' Heel of Breast Cancer: Mechanisms and Therapeutic Opportunities from a Comprehensive Systematic Review.International journal of molecular sciences · 2025Pooled it
- Revolutionizing breast cancer treatment: Harnessing the related mechanisms and drugs for regulated cell death (Review).International journal of oncology · 2024Pooled it
- Review of ferroptosis in colorectal cancer: Friends or foes?World journal of gastroenterology · 2023Pooled it
- Tumor cell ferroptosis in antitumor immunity and immunotherapy efficacy.Journal for immunotherapy of cancer · 2026Review
- Role of ferroptosis on immunotherapy in breast cancer.Molecular biology reports · 2026Review
- Co-Delivery of Ferrostatin-1 and M2 Macrophage-Derived Exosomal Signals via Engineered Hybrid Nanovesicles Enables Synergistic Neuroprotection in Traumatic Brain Injury.ACS applied materials & interfaces · 2026Article
- Subtype-Consistent Upregulation of Ferroptosis-Associated Pathways in Breast Cancer with Heterogeneous Prognostic Implications and Systemic Response to Cryoablation.International journal of molecular sciences · 2026Article
- Regulation of mitochondrial ROS by C15ORF48 in a basal cell subpopulation contributes to chemotherapy resistance in TNBC.Science advances · 2026Article
- GPX4 Inhibitor Resistance and Metastatic Features in Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting ferroptosis in cancer: from mechanistic insights to therapeutic approaches.Molecular biomedicine · 2026Review
- Sevoflurane-induced ferroptosis in developing neurons mediated by the NCOA4-ferritinophagy-GPX4 pathway.Journal of molecular histology · 2026Article
- Computational characterization of GRP78 binding sites on mitochondrial GPX4: implications for targeting ferroptosis in triple-negative breast cancer.Scientific reports · 2026Article
- Recent Advancements in Drug Targeting for Ferroptosis as an Antitumor Therapy: Development of Novel therapeutics.Current cancer drug targets · 2026Review
- Biochemical and Comparative Proteomic Analyses Delineate the Anti-Ovarian Carcinogenic Roles of Modified Calycosin.Food science & nutrition · 2026Article
- Distinct mechanisms of cell in breast cancer and their clinical implication.Cell biology and toxicology · 2025Review
- Integrating large-scale in vitro functional genomic screen and multi-omics data to identify novel breast cancer targets.Breast cancer research and treatment · 2025Article
- Adaptive multi-omics integration framework for breast cancer survival analysis.Scientific reports · 2025Article
- Metabolic Regulation of Ferroptosis in Breast Cancer.International journal of molecular sciences · 2025Review
- Polymorphisms in cancer-related genes and their association with breast cancer risk in Iranian women.Molecular biology reports · 2025Article
- Leveraging diverse cell-death patterns to predict to predict prognosis and immunotherapy in hepatocellular carcinoma.Discover oncology · 2025Article
33 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gefitinib resistance in triple negative breast cancer (TNBC) is a growing important concern. Glutathione peroxidase 4 (GPX4) is a main regulator of ferroptosis, which is pivotal for TNBC cell growth. We investigated GPX4-mediated ferroptosis in gefitinib sensitivity in TNBC. Gefitinib resistant TNBC cells MDA-MB-231/Gef and HS578T/Gef were constructed and treated with lentivirus sh-GPX4 and ferroptosis inhibitor ferrostatin-1. GPX4 expression, cell viability and apoptosis were detected. Malondialdehyde (MDA), glutathione (GSH), reactive oxygen species (ROS) levels were evaluated. The levels of ferroptosis-related proteins were detected. Subcutaneous tumor model was established in nude mice, and gefitinib was intraperitoneally injected to evaluate tumor growth, apoptosis, and Ki-67 expression. GPX4 was increased in gefitinib-resistant cells. After silencing GPX4, the inhibition rate of cell viability was increased, the limitation of colony formation ability was reduced, apoptosis rate was increased, and the sensitivity of cells to gefitinib was improved. After silencing GPX4, MDA and ROS production were increased, while GSH was decreased. Silencing GPX4 promoted ferroptosis. Inhibition of GPX4 promoted gefitinib sensitivity by promoting cell ferroptosis.
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