ArticleOncoTargets and therapy2020
Dihydroartemisinin Inhibits the Proliferation, Colony Formation and Induces Ferroptosis of Lung Cancer Cells by Inhibiting PRIM2/SLC7A11 Axis.
Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.
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Who cites it
68 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 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
- Cross-kingdom sRNA Ta_sRNA1 silences PRIM2 to fine-tune Arabidopsis immunity during symbiosis with Trichoderma atroviride.The New phytologist · 2026Article
- The Therapeutic Potential of Dihydroartemisinin in Cancer Treatment.International journal of molecular sciences · 2026Review
- Natural products in treating sepsis-associated lung and liver injuries by mediating ferroptosis, current progress, and future perspective.Frontiers in pharmacology · 2026Review
- High-Dose Ascorbic Acid Combined With Dihydroartemisinin Inhibits Lung Adenocarcinoma Malignancy by Inducing Ferroptosis via SLC7A11/GPX4 Pathway.Journal of cellular and molecular medicine · 2025Article
- Ferroptosis and non-coding RNAs in lung cancer: exploring molecular mechanisms and diagnostic/therapeutic implications.Cancer cell international · 2025Review
- The role of the NcRNA/ferroptosis axis in lung cancer: molecular mechanisms and potential therapeutic targets.Apoptosis : an international journal on programmed cell death · 2025Review
- A new perspective on iron-dependent cell death: PRDX-1-mediated ferroptosis in tumor cells.Apoptosis : an international journal on programmed cell death · 2025Review
- A ROS-Responsive Dual-Targeting Drug Nanocarrier Serving as a GSI Synergist and Ferroptosis Sensitizer for T-Cell Acute Lymphoblastic Leukemia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Hypofractionated radiotherapy (RT) combined with dihydroartemisinin (DHA): No synergistic effect observed in a preliminary animal study.Precision radiation oncology · 2025Article
- New Progress on DNA Primase Subunit Enzymes Research and Link to Cancer Development and Treatment Approaches.Current cancer drug targets · 2025Review
- Artemisinin and its derivatives: all-rounders that may prevent the progression from lung injury to lung cancer.Frontiers in pharmacology · 2025Review
- Natural products targeting ferroptosis in cancer: molecular mechanisms and applications.Frontiers in oncology · 2025Review
- Artemisinin derivatives maintain fibroblast normalization by acting on tumor-stroma interactions in oral tongue squamous cell carcinoma.American journal of cancer research · 2025Article
- Therapeutic Potential of Terpenoids in Cancer Treatment: Targeting Mitochondrial Pathways.Cancer reports (Hoboken, N.J.) · 2024Review
- Artemisinin and Its Derivatives as Potential Anticancer Agents.Molecules (Basel, Switzerland) · 2024Review
- Dihydroartemisinin restores the immunogenicity and enhances the anticancer immunosurveillance of cisplatin by activating the PERK/eIF2α pathway.Cell & bioscience · 2024Article
- [Effect and molecular mechanism of hesperadin-induced ferroptosis in chronic myeloid leukemia K562 cells].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2024Article
- Nicorandil Regulates Ferroptosis and Mitigates Septic Cardiomyopathy via TLR4/SLC7A11 Signaling Pathway.Inflammation · 2024Article
- Amino acid transporters within the solute carrier superfamily: Underappreciated proteins and novel opportunities for cancer therapy.Molecular metabolism · 2024Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveLung cancer is the first leading cause of cancer-related deaths both worldwide and in China and threatens human health and quality of life. New drugs and therapeutic methods are urgently needed. Our study evaluated the roles of dihydroartemisinin (DHA) in lung cancer and further explored its underlying mechanisms.
methodsCCK-8, colony formation and trypan blue exclusion assays were used to detect the cell viability, colony formation ability and cell death. qRT-PCR and Western blotting assays were applied to analyze the expressions of key molecules.
resultsDHA inhibited the proliferation and colony formation abilities and enhanced the cell death and induced ferroptosis of lung NCI-H23 and XWLC-05 cancer cells. DHA reduced PRIM2 expression and silencing PRIM2 mimicked the inhibitory roles on proliferation and colony formation and promotive roles on cell death and ferroptosis of DHA in lung NCI-H23 and XWLC-05 cancer cells. We further found that DHA treatment and loss of PRIM2 reduced the GSH level and increased the cellular lipid ROS and mitochondrial MDA levels, and further downregulated the expressions of SLC7A11 and β-catenin in lung cancer cells, respectively. Exogenetic overexpression of PRIM2 recovered the inhibitory effects of DHA on proliferation and colony formation in lung NCI-H23 cancer cells, meanwhile loss of PRIM2 sensitizes NCI-H23 cells to DHA therapy. In vivo experiment further showed that DHA treatment significantly suppressed the tumor growth and downregulated PRIM2 and SLC7A11.
conclusionOur study suggested that DHA inhibited the proliferation, colony formation and enhanced cell death and induced ferroptosis of lung cancer cells by inactivating PRIM2/SLC7A11 axis. Loss of PRIM2 induced ferroptosis might developed to be a novel therapeutic method in lung cancer therapy.
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