ArticleWorld journal of surgical oncology2024
Inhibition of HOXC11 by artesunate induces ferroptosis and suppresses ovarian cancer progression through transcriptional regulation of the PROM2/PI3K/AKT pathway.
Article in World journal of surgical oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- The evaluation of biological effects of artesunate on ovarian cancer using three-dimensional cell culture methods.Cell and tissue banking · 2026Article
- Synthesis and Biological Evaluation of Isomeric Artemisinin Trimers as Novel Antitumor Agents.Molecules (Basel, Switzerland) · 2026Article
- Advances in ferroptosis research in ovarian cancer: molecular mechanisms and therapeutic perspectives.American journal of cancer research · 2026Review
- PROM2 exacerbates CCl4-Induced liver fibrosis via NLRP3 inflammasome activation and hepatocyte pyroptosis.Cellular and molecular life sciences : CMLS · 2025Article
- Multi-Omics analysis and in vitro validation reveal diagnostic and therapeutic roles of novel hub genes in ovarian cancer.Hereditas · 2025Article
- CircASH1L inhibits ferroptosis and enhances cisplatin resistance by sponging miR-515-5p to regulate cell cycle-related CDCA7/RRM2 in ovarian cancer cells.Frontiers in pharmacology · 2025Article
- Artemisiae Annuae Herba: from anti-malarial legacy to emerging anti-cancer potential.Theranostics · 2025Review
- Targeting ferroptosis: a promising avenue for ovarian cancer treatment.Frontiers in immunology · 2025Review
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8 authors.
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Abstract
backgroundFerroptosis, a non-apoptotic form of regulated cell death, plays a critical role in the suppression of various tumor types, including ovarian cancer. Artesunate (ART), a derivative of artemisinin, exhibits extensive antitumor effects and is associated with ferroptosis. This study aimed to investigate the mechanisms through which ART induces ferroptosis to inhibit ovarian cancer.
methodsRNA sequencing was conducted to identify differentially expressed genes associated with ART-induced ferroptosis. Dual-luciferase reporter assays and electrophoretic mobility shift assays were performed to confirm the interaction between Homeobox C11 (HOXC11) and the Prominin 2 (PROM2) promoter. Cell Counting Kit-8 (CCK-8) assays, flow cytometry, and wound healing assays were used to analyze the antitumor effects of ART. Western blot, biochemical assays and transmission electron microscope were utilized to further characterize ART-induced ferroptosis. In vivo, the effects of ART on ferroptosis were examined using a xenograft mouse model.
resultsRNA sequencing analysis revealed that the HOXC11, PROM2 and Phosphatidylinositol 3-Kinase/ Protein Kinase B (PI3K/AKT) pathways were downregulated by ART. HOXC11 was found to regulate PROM2 expression by binding to its promoter directly. HOXC11 overexpression reversed ART-induced effects on ovarian cancer cell proliferation, migration, apoptosis and ferroptosis by activating the PROM2/PI3K/AKT signaling axis. Conversely, silencing PROM2 in HOXC11-overexpressing cells restored ART-induced ferroptosis and its associated antitumor effects by inhibiting the PI3K/AKT pathway. Consistently, in vivo studies using a xenograft mouse model confirmed that ART-induced tumor inhibition was mediated by ferroptosis through the suppression of the HOXC11/PROM2/PI3K/AKT pathway.
conclusionThis study identifies the HOXC11/PROM2/PI3K/AKT axis as a novel regulatory mechanism underlying ART-induced ferroptosis in ovarian cancer. Targeting the HOXC11/PROM2 axis may represent a promising therapeutic strategy for enhancing ferroptosis, offering new insights for the treatment of ovarian cancer.
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