Astragaloside IV represses hepatocellular carcinoma progression by modulating HMGB1-ferroptosis axis
- PMID: 40751851
- PMCID: PMC12317954
- DOI: 10.1007/s12672-025-03286-5
Astragaloside IV represses hepatocellular carcinoma progression by modulating HMGB1-ferroptosis axis
Abstract
Astragaloside IV (AST-IV), as one of the main functional components of Astragalus membranaceus, has physiological functions such as regulating metabolism and anti-tumor. However, the role of AST-IV on hepatocellular carcinoma (HCC) was still poorly understood. In this study, our work explored whether AST-IV could induce ferroptosis and repress HCC tumorigenesis. Results indicated that AST-IV could repress the tumor progression (viability, migration) of HCC in vitro. Besides, AST-IV induced the ferroptosis (Fe2+, malondialdehyde, lipid peroxidation) in HCC cells. Molecular docking and microscale thermophoresis indicated that high mobility group protein B1 (HMGB1) acted as the target of AST-IV. AST-IV could repress the HMGB1 expression and HMGB1 reversed the role of AST-IV on HCC cells' ferroptosis. In vivo, AST-IV administration repressed the tumor progression. In conclusion, AST-IV represses HCC progression by modulating HMGB1-ferroptosis axis, which provides a novel insight for HCC.
Keywords: Astragaloside IV; Ferroptosis; HMGB1; Hepatocellular carcinoma.
© 2025. The Author(s).
Conflict of interest statement
Declarations. Ethics approval and consent to participate: All animal protocol and details in present study had been conducted in accordance with the ethical principles and guidelines of the International Council for Laboratory Animal Science (ICLAS). The study had been approved by the Ethical Committee of Guangdong Provincial People’s Hospital. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests. Clinical trial number: Not applicable.
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