ArticleJournal of advanced research2025
Salidroside sensitizes Triple-negative breast cancer to ferroptosis by SCD1-mediated lipogenesis and NCOA4-mediated ferritinophagy.
Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed.
- Research progress of ferroptosis in gynecological diseases.Annals of medicine · 2026Review
- P38α deficiency alleviates myocardial ischemia/reperfusion injury by stabilizing c‑Myc to inhibit ferroptosis.Basic research in cardiology · 2026Article
- The pivotal role of SCD1 in digestive cancers: Bridging lipid metabolic reprogramming and programmed cell death (Review).International journal of oncology · 2026Review
- Beyond conventional therapies: the evolution of targeted agents and immunotherapies in triple-negative breast cancer.Acta pharmacologica Sinica · 2026Review
- Article
- A fungal-derived benzothiazole derivative overcomes osimertinib resistance in NSCLC by targeting SCD1.Natural products and bioprospecting · 2026Article
- S100A9 modulates USP7-mediated stabilization of NCOA4 to promote ferroptosis in sepsis-associated acute lung injury.Redox biology · 2026Article
- [Overexpression of miR-183-5p enhances malignant phenotype and inhibits ferroptosis of triple-negative breast cancer cells by negatively regulating KLHL24].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Timosaponin AIII-based liposomes loaded with Auranofin for the induction of ferroptosis in anaplastic thyroid carcinoma.Journal of cancer research and clinical oncology · 2026Article
- PRRC2A-mediated mCell death & disease · 2026Article
- FerroScore: a statistical approach for quantifying tumor-related ferroptosis based on omics data.Briefings in bioinformatics · 2026Article
- Targeting the fibrosis-inflammation-oxidative stress axis: multifaceted mechanisms of salidroside in chronic organ fibrosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Stearoyl-CoA desaturase 1 integrates tissue-specific oncogenic pathways into a pan-cancer ferroptosis resistance program.Cell death & disease · 2026Review
- Intestinal Epithelial Cell Ferroptosis in Ulcerative Colitis: Pathogenesis, Signaling Networks, and Therapeutic Implications.Current medical science · 2026Review
- A highly biocompatible self-assembled Pt(IV) nanoplatform integrating Nrf2 inhibition for synergistic apoptosis and ferroptosis in hepatocellular carcinoma.Materials today. Bio · 2026Article
- Ferroptosis in breast cancer: From adipocyte-immune-iron regulation to therapeutic application.Clinical and translational medicine · 2026Review
- Hesperetin-black phosphorus nanosheets targeting TAMs induce ferroptosis and reverse protumoral polarization to remodel the immune microenvironment.Materials today. Bio · 2026Article
- NCOA4-driven ferritinophagy and GSH reprogramming underlie maslinic acid-induced ferroptosis and autophagy in breast cancer.Translational cancer research · 2026Article
- Single-cell N4-acetylcytidine regulatory landscape identifies ARIH1 as a ferroptosis-suppressive oncogenic driver in lung adenocarcinoma.Respiratory research · 2026Article
- Awakening endogenous repair: salidroside boosts mitophagy in NPMSCs via SIRT1/FOXO3 to combat intervertebral disc degeneration.Stem cell research & therapy · 2026Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionTriple-negative breast cancer (TNBC) is the primary cause of breast cancer-induced death in women. Literature has confirmed the benefits of Salidroside (Sal) in treating TNBC. However, the study about potential therapeutic targets and mechanisms of Sal-anchored TNBC remains limited.
objectiveThis study was designed to explore the main targets and potential mechanisms of Sal against TNBC.
methodsNetwork pharmacology, bioinformatics, and machine learning algorithm strategies were integrated to examine the role, potential targets, and mechanisms of the Sal act in TNBC. MDA-MB-231 cells and tumor-bearing nude mice were chosen for in vitro and in vivo experimentation. Cell viability and cytotoxicity were determined using CCK-8, LDH test, and Calcein-AM/PI staining. Antioxidant defense, lipid peroxidation, and iron metabolism were explored using glutathione, glutathione peroxidase, malondialdehyde (MDA), C11-BODIPY 581/591 probe, and FerroOrange dye. Glutathione peroxidase 4 (GPX4) or stearoyl-CoA desaturase 1 (SCD1) overexpression or nuclear receptor co-activator 4 (NCOA4) deficiency was performed to demonstrate the mechanism of Sal on TNBC.
resultsThe prediction results confirmed that 22 ferroptosis-related genes were identified in Sal and TNBC, revealing that the potential mechanism of the Sal act on TNBC was linked with ferroptosis. Besides, these genes were mainly involved in the mTOR, PI3K/AKT, and autophagy signaling pathway by functional enrichment analysis. The in vitro validation results confirmed that Sal inhibited TNBC cell proliferation by modulating ferroptosis via elevation of intracellular Fe
conclusionsOverall, this study elucidates TNBC pathogenesis closely linked to ferroptosis and identifies potential biomarkers in TNBC. Meanwhile, the study elucidates that Sal sensitizes TNBC to ferroptosis by SCD1-mediated lipogenesis and NCOA4-mediated ferritinophagy, regulated by PI3K/AKT/mTOR signaling pathways. Our findings provide a theoretical basis for applying Sal to treat TNBC.
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