ArticleFrontiers in molecular biosciences2023
Susceptibility of cervical cancer to dihydroartemisinin-induced ferritinophagy-dependent ferroptosis.
Article in Frontiers in molecular biosciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- The Role of Artemisinin and its Derivatives in Cancer Therapy via Ferroptosis: A Systematic Review ofAnti-cancer agents in medicinal chemistry · 2026Pooled it
- Research progress of ferroptosis in gynecological diseases.Annals of medicine · 2026Review
- Lyssavirus Nucleoprotein Induces GPAT4-Mediated CYB5R1 Depalmitoylation to Suppress Ferroptosis and Promote Viral Replication.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Desmoglein 2 is associated with dihydroartemisinin resistance in HeLa cervical cancer cells: a potential link to the PI3K/AKT signaling pathway.Discover oncology · 2026Article
- RNF112 mediates immunosuppression to inhibit the proliferation of cervical cancer by Foxm1.Translational cancer research · 2026Article
- The Therapeutic Potential of Dihydroartemisinin in Cancer Treatment.International journal of molecular sciences · 2026Review
- Synthesis and Biological Evaluation of Isomeric Artemisinin Trimers as Novel Antitumor Agents.Molecules (Basel, Switzerland) · 2026Article
- Heme as activator and target for artemisinin: Towards multiple pharmacological bioactivity.Biochemistry and biophysics reports · 2026Review
- Ferritinophagy as a Double-Edged Sword in Cancer: Novel Insights into Therapeutic Targeting of Iron-Driven Ferroptosis.Cell biochemistry and biophysics · 2026Review
- HPV-driven metabolic reprogramming promotes T cell exhaustion: targeting immunometabolic barriers with natural products.Frontiers in immunology · 2026Review
- From molecular crosstalk to precision therapy: targeting ferroptosis and cuproptosis in oral squamous cell carcinoma.Frontiers in oncology · 2026Review
- Combined Dihydroartemisinin and Eupatilin Suppress Prostate Cancer through AR-Associated Ferroptosis and Modulation of Macrophage-Tumor Crosstalk.Research (Washington, D.C.) · 2026Article
- Targeting metalloptosis in tumor therapy: from molecular mechanisms to application of metal nanoparticles.Molecular cancer · 2025Review
- Regulation of iron metabolism in ferroptosis: From mechanism research to clinical translation.Journal of pharmaceutical analysis · 2025Review
- Ferroptosis as a therapeutic target in glioblastoma: Mechanisms and emerging strategies.Molecular therapy. Nucleic acids · 2025Review
- Artemisinin and Its Derivatives from Molecular Mechanisms to Clinical Applications: New Horizons Beyond Antimalarials.International journal of molecular sciences · 2025Review
- Nrf2/UBE3B protects against acute lung injury by inhibiting ferritinophagy through the ubiquitination of NCOA4.Biology direct · 2025Article
- Targeting ferroptosis for precision medicine in cervical cancer.Apoptosis : an international journal on programmed cell death · 2025Review
- Interactions between ferroptosis and tumour development mechanisms: Implications for gynaecological cancer therapy (Review).Oncology reports · 2025Review
- Ferroptosis-immune crosstalk in cervical cancer: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The clinical therapeutics of cervical cancer is limited due to the drug resistance and metastasis of tumor. As a novel target for antitumor therapy, ferroptosis is deemed to be more susceptible for those cancer cells with resistance to apoptosis and chemotherapy. Dihydroartemisinin (DHA), the primary active metabolites of artemisinin and its derivatives, has exhibited a variety of anticancer properties with low toxicity. However, the role of DHA and ferroptosis in cervical cancer remained unclear. Here, we showed that DHA could time-dependently and dose-dependently inhibit the proliferation of cervical cancer cells, which could be alleviated by the inhibitors of ferroptosis rather than apoptosis. Further investigation confirmed that DHA treatment initiated ferroptosis, as evidenced by the accumulation of reactive oxygen species (ROS), malondialdehyde (MDA) and liquid peroxidation (LPO) levels and simultaneously depletion of glutathione peroxidase 4 (GPX4) and glutathione (GSH). Moreover, nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy was also induced by DHA leading to subsequent increases of intracellular labile iron pool (LIP), exacerbated the Fenton reaction resulting in excessive ROS production, and enhanced cervical cancer ferroptosis. Among them, we unexpectedly found that heme oxygenase-1 (HO-1) played an antioxidant role in DHA-induced cell death. In addition, the results of synergy analysis showed that the combination of DHA and doxorubicin (DOX) emerged a highly synergistic lethal effect for cervical cancer cells, which was related also to ferroptosis. Overall, our data revealed the molecular mechanisms that DHA triggered ferritinophagy-dependent ferroptosis and sensitized to DOX in cervical cancer, which may provide novel avenues for future therapy development.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.