ArticleOncology reports2021
Dihydroartemisinin triggers ferroptosis in primary liver cancer cells by promoting and unfolded protein response‑induced upregulation of CHAC1 expression.
Article in Oncology reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 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
- Bufalin Suppresses Pancreatic Ductal Adenocarcinoma Through ER Stress-Ferroptosis Crosstalk Associated with IPInternational journal of molecular sciences · 2026Article
- The Therapeutic Potential of Dihydroartemisinin in Cancer Treatment.International journal of molecular sciences · 2026Review
- H3K9 acetylation-dependent CHAC1 transcription in dihydroartemisinin-induced hepatic stellate cell ferroptosis.Chinese medical journal · 2026Article
- FoxO3a-Mediated Modulation of PD-L1 Expression and Inhibition by Dihydroartemisinin in Triple-Negative Breast Cancer.Journal of cellular and molecular medicine · 2026Article
- Metabolic cell deaths in head and neck cancer: mechanisms, therapeutic potential, and challenges.Annals of medicine · 2025Review
- The Unfolded Protein Response-Novel Mechanisms, Challenges, and Key Considerations for Therapeutic Intervention.Cancers · 2025Review
- Melatonin-induced ferroptosis in pancreatic cancer cells by stimulating endoplasmic reticulum stress and inhibiting alanine-serine-cysteine transporter 2-driven glutamine metabolism.World journal of gastroenterology · 2025Article
- Natural anti-cancer products: insights from herbal medicine.Chinese medicine · 2025Review
- Protein S-glutathionylation confers cellular resistance to ferroptosis induced by glutathione depletion.Redox biology · 2025Article
- The marine xanthophyll diatoxanthin as ferroptosis inducer in MDAMB231 breast cancer cells.Scientific reports · 2025Article
- Roles of X-box binding protein 1 in liver pathogenesis.Clinical and molecular hepatology · 2025Review
- Caffeic Acid Reduces Ferroptosis to Dampen Inflammation of Keratinocytes in Psoriasis by Inhibiting EGR1-induced Transcription Activation of CHAC1.Current molecular medicine · 2025Article
- The strategic breakdown: CHAC enzymes as regulators of glutathione homeostasis and disease implications.Frontiers in molecular biosciences · 2025Review
- Natural products targeting ferroptosis in cancer: molecular mechanisms and applications.Frontiers in oncology · 2025Review
- Artemisiae Annuae Herba: from anti-malarial legacy to emerging anti-cancer potential.Theranostics · 2025Review
- Artemisinin derivatives maintain fibroblast normalization by acting on tumor-stroma interactions in oral tongue squamous cell carcinoma.American journal of cancer research · 2025Article
- Mechanism of cell death and its application in the repair of inflammatory bowel disease by mesenchymal stem cells.Frontiers in immunology · 2025Review
- Ferroptosis: insight into the treatment of hepatocellular carcinoma.Cancer cell international · 2024Review
- CHAC1 blockade suppresses progression of lung adenocarcinoma by interfering with glucose metabolism via hijacking PKM2 nuclear translocation.Cell death & disease · 2024Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dihydroartemisinin (DHA), an artemisinin derivate, has been investigated as a potential antitumor drug in primary liver cancer (PLC). Ferroptosis is a form of iron‑dependent cell death that can be driven by lipid peroxidation inducers. The present study aimed to determine whether and how DHA could promote the death of PLC cells by inducing ferroptosis. In total, four PLC cell lines with different p53 statuses, including Hep3B (p53 null), Huh7 (p53 mutant), PLC/PRF/5 (p53 mutant) and HepG2 (p53 wild‑type), were treated with various concentrations of DHA. The effects of DHA on all three branches of the unfolded protein response (UPR) were evaluated. To deactivate the UPRs, small interfering RNA was used to knockdown the expression of activating transcription factor (ATF)4, X‑box binding protein 1 (XBP1) or ATF6 in PLC cells. The effect of DHA on the promoter activity of Chac glutathione specific γ‑glutamylcyclotransferase 1 (CHAC1) was evaluated using a dual luciferase reporter assay. The results revealed that DHA‑induced death in PLC cells was irrelevant of the p53 status. PLC cells exposed to DHA displayed classic features of ferroptosis, such as increased lipid reactive oxygen species and malondialdehyde levels, an iron overload, and decreased activity or expression of glutathione (GSH), glutathione peroxidase 4, solute carrier family (SLC) 7 member 11 and SLC family 3 member 2. The antitumor effects of DHA in PLC cells were significantly weakened by two typical ferroptosis inhibitors, ferrostatin‑1 and deferoxamine mesylate salt, whereas the antitumor effects were augmented following iron overload. Furthermore, DHA activated all three branches of the UPR (eukaryotic translation initiation factor 2 α kinase 3/eukaryotic translation initiation factor 2A/ATF4, inositol‑requiring transmembrane kinase/endoribonuclease 1α/XBP1 and ATF6 branches)
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