ArticleAmerican journal of translational research2024
Bavachin stimulates ferroptosis and reduces malignant phenotype progression of hepatocellular carcinoma cells by inducing lipid peroxidation by modulation of the Nrf2/HO-1 signaling pathway.
Article in American journal of translational research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- A bezafibrate bearing Pt(IV) prodrug triggers ferroptosis via modulating lipid metabolism in lung cancer cells.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2026Article
- Phytochemical basis and antitumor mechanisms ofFrontiers in immunology · 2026Review
- Targeting ferroptosis as a therapeutic strategy for hepatotoxicity.Toxicology reports · 2025Review
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6 authors.
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Abstract
backgroundThe mechanism of ferroptosis is primarily driven by the iron-dependent lethal accumulation of membrane lipid peroxidation. Bavachin has been found to exacerbate lipid peroxidation in cancer cells; however, whether it hinders hepatocellular carcinoma (HCC) progression by way of ferroptosis remains unknown.
methodsCell counting kit-8 (CCK-8) assay was used to measure the effect of Bavachin on the viability of HCC cells, so as to determine the appropriate drug concentration for subsequent experiments. Combining molecular biology experimental techniques such as CCK-8, flow cytometry, western blotting, wound-healing assay, DCFH-DA (2',7'-dichlorodihydrofluorescein diacetate) fluorescent probe and a variety of biological kits, the effects of Bavachin on HCC cell malignant phenotype progression and ferroptosis were investigated.
resultsBavachin significantly induced cytotoxicity of Huh-7 and HepG2 cells at concentrations of 20 and 40 μM, respectively. Bavachin intervention prominently reduced cell proliferation and migration, and enhanced cell apoptosis in HCC. Also, Bavachin enhanced the process of lipid peroxidation, as indicated by increased reactive oxygen species (ROS), lipid peroxidation (LPO) and malondialdehyde (MDA) production, and decreased superoxide dismutase (SOD) and glutathione (GSH) production. Ferrostin-1, a ferroptosis inhibitor, reduced the Bavachin-induced cell survival rate. Bavachin intervention induced ferroptosis by enhancing iron ion concentration, acyl-CoA synthetase long-chain family member 4 (ACSL4) expression, and reducing glutathione peroxidase-4 (GPX4) expression. Bavachin exerted anti-cancer effects though inducing ferroptosis by activating the nuclear factor erythroid 2-related factor 2 (Nrf2)/Heme oxygenase-1 (HO-1) pathway.
conclusionBavachin acted as a ferroptosis inducer, promoted ROS release, enhanced lipid peroxidation, and inhibited HCC cell malignant phenotype progression by modulating the Nrf2/HO-1 pathway.
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