ArticleFrontiers in pharmacology2025
Cepharanthine hydrochloride: a novel ferroptosis-inducing agent for prostate cancer treatment.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Ethnobotanical study on medicinal plants used by Jinuo people in Yunnan, China.Journal of ethnobiology and ethnomedicine · 2026Article
- Androgen receptor signaling organizes ferroptosis escape in castration-resistant prostate cancer: a threshold-based model for therapeutic timing.Frontiers in oncology · 2026Review
- Cepharanthine Induces Oxidative Stress and Apoptosis in Cervical Cancer via the Nrf2/Keap1 Pathway.Antioxidants (Basel, Switzerland) · 2025Article
- Integration of network pharmacology, transcriptomics, and experimental verification to investigate the mechanism of action of cepharanthine hydrochloride against prostate cancer.Scientific reports · 2025Article
- Cepharanthine hydrochloride inhibits prostate cancer progression by modulating gut microbiota and metabolites.Frontiers in pharmacology · 2025Article
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9 authors.
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Abstract
Background: Ferroptosis is an intracellular iron-dependent cell death that is distinct from apoptosis, necrosis, and autophagy. Increasing evidence indicated that ferroptosis plays a crucial role in suppressing tumors, thus providing new opportunities for cancer therapy. The drug cepharanthine, commonly used to treat leukopenia, has been discovered to function as an anticancer agent to multiple types of cancer via diverse mechanisms. However, the effect of cepharanthine on prostate cancer remains unclear. Methods: A semi-synthetic derivative of cepharanthine, cepharanthine hydrochloride (CH), is used in this study due to its better water solubility and bioavailability. The prostate cancer cell lines LNCaP, 22Rv1, PC3 and xenograft mouse models are used for detecting the anti-tumor effect of CH Results: CH inhibits cellular functions and trigger ferroptosis in prostate cancer cells. Mechanistic research revealed both common and distinct pharmacological mechanisms of CH-induced ferroptosis in different prostate cancer cells. High-throughput transcriptome analysis revealed that ferroptosis-related genes are significantly regulated in androgen receptor-dependent cells 22Rv1 and LNCaP, and less significantly in androgen receptor-independent cell PC3. Furthermore, CH was found to reduce the gene expressions and protein levels of GPX4 and FSP1 through modulating the activity of the androgen receptor signaling pathway, but not through its transcription factor activity. In addition, CH upregulated ACSL4 and downregulated DHODH, with the combined regulatory outcomes synergistically inducing ferroptosis. An Conclusion: This study has identified CH as a novel ferroptosis-inducing agent for the treatment of prostate cancer. The multiple mechanisms we found provides strong evidence for the eventual clinical application of the drug.
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