ArticleMolecular and cellular biochemistry2026
S-equol promotes ferroptosis in triple negative breast cancer by coordinating NCOA4-mediated ferritinophagy and PPARγ-mediated lipid metabolism.
Article in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Transcriptome Sequencing Reveals That Curcumin Protects Leghorn Chicken Cardiomyocytes from Heat Stress-Induced Iron Dysregulation.Animals : an open access journal from MDPI · 2026Article
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7 authors.
Funding
Abstract
Triple negative breast cancer (TNBC) is a diverse and highly aggressive cancer characterized by a strong tendency to metastasize, poor prognosis, and a lack of effective therapeutic targets. S-equol, an active metabolinte produced by gut microbiota through the conversion of daidzein, has been proven to possess anticancer activity. This study aims to investigate the anticancer effects of S-equol on TNBC and to elucidate key targets and potential mechanisms. In vitro experiments utilized the TNBC cell lines, while in vivo experiments employed a nude mouse xenograft tumor model. By means of using CCK-8, colony formation, scratch, and transwell invasion assays, the biological function of S-equol was evaluated. In addition, bioinformatics methods were employed to explore the potential signaling pathways and target genes of S-equol. The in vitro results substantiated that S-equol significantly suppressed both the proliferation and metastatic capacity of TNBC cells. Moreover, the prediction results indicated that S-equol may exert its anti-TNBC effects through ferroptosis via the PI3K/AKT signaling pathway, with PPARγ identified as the key gene. In vitro and in vivo results collectively verified that S-equol triggers ferroptosis by influencing lipid peroxidation and Fe²
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