ArticleAntioxidants (Basel, Switzerland)2022
Vulnerability of Triple-Negative Breast Cancer to Saponin Formosanin C-Induced Ferroptosis.
Article in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- Emerging role of plant-based compounds as ferroptosis modulators in breast cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Bufalin Suppresses Pancreatic Ductal Adenocarcinoma Through ER Stress-Ferroptosis Crosstalk Associated with IPInternational journal of molecular sciences · 2026Article
- Ferritinophagy as a Double-Edged Sword in Cancer: Novel Insights into Therapeutic Targeting of Iron-Driven Ferroptosis.Cell biochemistry and biophysics · 2026Review
- Co-targeting ferroptosis and immune evasion through small molecules in breast cancer.Journal of translational internal medicine · 2025Article
- Lipid reprogramming and ferroptosis crosstalk in clear cell renal cell carcinoma: metabolic vulnerabilities and therapeutic targeting.Molecular cancer · 2025Review
- Natural Compounds as Modulators of Ferroptosis: Mechanistic Insights and Therapeutic Prospects in Breast Cancer.Biomolecules · 2025Review
- Ferroptosis in TNBC: interplay with tumor-infiltrating immune cells and therapeutic implications.Molecular and cellular biochemistry · 2025Review
- Using Integrated Bioinformatics Analysis to Identify Saponin Formosanin C as a Ferroptosis Inducer in Colorectal Cancer with p53 and Oncogenic KRAS.Antioxidants (Basel, Switzerland) · 2025Article
- Salidroside sensitizes Triple-negative breast cancer to ferroptosis by SCD1-mediated lipogenesis and NCOA4-mediated ferritinophagy.Journal of advanced research · 2025Article
- Agapanthussaponin A from the Underground Parts ofMolecules (Basel, Switzerland) · 2025Article
- Formosanin C inhibits triple-negative breast cancer progression by suppressing the phosphorylation of STAT3 and the polarization of M2 macrophages.Breast cancer research and treatment · 2025Article
- Targeting the initiator to activate both ferroptosis and cuproptosis for breast cancer treatment: progress and possibility for clinical application.Frontiers in pharmacology · 2024Review
- Novel Insights on Ferroptosis Modulation as Potential Strategy for Cancer Treatment: When Nature Kills.Antioxidants & redox signaling · 2024Review
- Ferroptosis and its impact on common diseases.PeerJ · 2024Review
- Ferritinophagy: research advance and clinical significance in cancers.Cell death discovery · 2023Review
- Formosanin C suppresses cancer cell proliferation and migration by impeding autophagy machinery.The Kaohsiung journal of medical sciences · 2023Article
- Compounds targeting ferroptosis in breast cancer: progress and their therapeutic potential.Frontiers in pharmacology · 2023Review
- Ferroptosis and mitochondrial dysfunction in acute central nervous system injury.Frontiers in cellular neuroscience · 2023Review
- Phytochemicals Targeting Ferroptosis: Therapeutic Opportunities and Prospects for Treating Breast Cancer.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Targeting ferritin via autophagy (ferritinophagy) to induce ferroptosis, an iron- and reactive oxygen species (ROS)-dependent cell death, provides novel strategies for cancer therapy. Using a ferroptosis-specific inhibitor and iron chelator, the vulnerability of triple-negative breast cancer (TNBC) MDA-MB-231 cells to ferroptosis was identified and compared to that of luminal A MCF-7 cells. Saponin formosanin C (FC) was revealed as a potent ferroptosis inducer characterized by superior induction in cytosolic and lipid ROS formation as well as GPX4 depletion in MDA-MB-231 cells. The FC-induced ferroptosis was paralleled by downregulation of ferroportin and xCT expressions. Immunoprecipitation and electron microscopy demonstrated the involvement of ferritinophagy in FC-treated MDA-MB-231 cells. The association of FC with ferroptosis was strengthened by the results that observed an enriched pathway with differentially expressed genes from FC-treated cells. FC sensitized cisplatin-induced ferroptosis in MDA-MB-231 cells. Through integrated analysis of differentially expressed genes and pathways using the METABRIC patients' database, we confirmed that autophagy and ferroptosis were discrepant between TNBC and luminal A and that TNBC was hypersensitive to ferroptosis. Our data suggest a therapeutic strategy by ferroptosis against TNBC, an aggressive subtype with a poor prognosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.