ArticleAnimal models and experimental medicine2025
Brassinin from Brassica campestris L. inhibits colorectal cancer by inducing p62/NRF2/GPX4-regulated ferroptosis.
Article in Animal models and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Knocking down FAM110A suppresses colon adenocarcinoma progression by inhibiting the Nrf2/HO-1 axis to induce ferroptosis.World journal of surgical oncology · 2026Article
- Mechanism of AGEs-RAGE axis inhibition of ferroptosis in type 2 diabetic colon cancer by regulatory CEACAM1.Scientific reports · 2026Article
- Shenqi Granules Enhance Recovery from Myocardial Ischemia-Reperfusion Injury by Downregulating MMP9 and ADH1C.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Natural products targeting the Nrf2 signaling pathway: potential targets and intervention strategies for the prevention and treatment of colorectal cancer.Frontiers in pharmacology · 2026Review
- Brassinin Induces HMolecules (Basel, Switzerland) · 2025Article
- Brassinin from Brassica campestris L. inhibits colorectal cancer by inducing p62/NRF2/GPX4-regulated ferroptosis.Animal models and experimental medicine · 2025Article
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6 authors.
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Abstract
backgroundIndole phytoalexins, plant-derived compounds present in cruciferous vegetables, have demonstrated anticancer properties. Brassinin (BSN), derived from Brassica campestris L. var. campestris, is known for its potent antitumor effects on various cancers. However, the role of ferroptosis in regulating the antitumor effects of BSN has not been fully elucidated.
methodsThe components of B. campestris L. against colorectal cancer (CRC) were analyzed by network pharmacology. CCK-8 assay and colony formation assay detected cell viability induced by BSN. Molecular docking verified the binding of BSN to the target protein. Western blot and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) assay revealed whether BSN can inactivate the NRF2 signaling and inhibit the expression of p62 and HO-1. The RKO-xenograft tumor models were established and then were treated by 75 or 150 mg/kg BSN to verify the antitumor efficacy and side effects of BSN.
resultsNetwork pharmacology suggested that BSN is the most important component of B. campestris L. against CRC. BSN inhibits CRC cell viability in a dose- and time-dependent manner. Furthermore, this inhibitory effect is associated with the induction of ferroptosis, as BSN suppresses the cell viability of CRC by inducing GPX4-regulated ferroptosis. BSN may bind to NRF2 protein to inactivate the NRF2 signaling, inhibiting the expression of p62 and HO-1. Importantly, a low dose or a high dose of BSN significantly reduced the tumor growth in vivo.
conclusionsOur findings reveal that BSN blocks CRC growth by inducing p62/NRF2/GPX4-regulated ferroptosis, which may be a novel lead compound for tumor treatment.
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