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- W4210365553 endingPage "298" @default.
- W4210365553 startingPage "298" @default.
- W4210365553 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." @default.
- W4210365553 created "2022-02-08" @default.
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- W4210365553 date "2022-01-31" @default.
- W4210365553 modified "2023-10-11" @default.
- W4210365553 title "Vulnerability of Triple-Negative Breast Cancer to Saponin Formosanin C-Induced Ferroptosis" @default.
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- W4210365553 doi "https://doi.org/10.3390/antiox11020298" @default.
- W4210365553 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35204181" @default.
- W4210365553 hasPublicationYear "2022" @default.
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