ArticleTranslational cancer research2026
NCOA4-driven ferritinophagy and GSH reprogramming underlie maslinic acid-induced ferroptosis and autophagy in breast cancer.
Article in Translational cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Breast cancer is the most prevalent cancer globally, with limited efficacy of traditional therapies and high drug resistance. Maslinic acid (MA) has broad-spectrum anti-tumor activity. This study aimed to investigate whether MA exerts its anti-tumor effects in breast cancer by inducing ferroptosis and autophagy. Methods: Breast cancer cell proliferation was assessed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and 5-ethynyl-2'-deoxyuridine (EdU) assays. Autophagy was evaluated by monitoring microtubule-associated protein 1A/1B-light chain 3 (LC3) expression and sequestosome 1 (p62) levels, combined with mRFP-GFP-LC3 plasmid transfection assay. MA-induced ferroptosis was investigated by measuring reactive oxygen species (ROS), glutathione (GSH), glutathione disulfide (GSSG), Glu, and Fe Results: MA significantly inhibited breast cancer cell proliferation. It activated autophagy in MDA-MB-231 cells autophagy by upregulating tumor protein p53 (p53) expression and inhibiting mammalian target of rapamycin (mTOR) signaling, evidenced by increased levels of beclin 1 (BECN1), unc-51 like autophagy activating kinase 1 (ULK1), autophagy protein 5 (ATG5), and phosphatidylethanolamine-conjugated LC3 (LC3-II), as well as decreased p62 expression, indicating enhanced autophagic flux. Meanwhile, MA induced MDA-MB-231 cell ferroptosis, characterized by elevated ROS, decreased GSH levels, and downregulated expression of glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11). Furthermore, MA increased Fe Conclusions: In MDA-MB-231 cells, MA triggered autophagy through p53 upregulation and mTOR signaling inhibition, and induced ferroptosis by reprogramming GSH metabolism and activating the NCOA4-mediated ferritinophagy pathway, lead to FTH1 degradation.
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