ArticleEuropean journal of medical research2024
Antitumour effects of artesunate via cell cycle checkpoint controls in human oesophageal squamous carcinoma cells.
Article in European journal of medical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Artesunate directly targeting MMP9 to reduce angiogenesis and increase CD8 + T cell infiltration inhibits hepatocellular carcinoma.Cancer cell international · 2026Article
- Anticancer properties of Artemisia species: mechanisms and experimental evidence.Molecular biology reports · 2026Review
- Teniposide Triggers DNA Repair Inhibition by Binding and Ubiquitination of Apurinic/Apyrimidinic Endonuclease 1 to Boost Oxidative DNA Damage for Lung Cancer Destruction.ACS pharmacology & translational science · 2025Article
- Safety and pharmacokinetics of FCN-437c, a novel cyclin-dependent kinase 4/6 inhibitor, in Chinese patients with hepatic impairment.Investigational new drugs · 2025Article
- Article
- Artemisinin and Its Derivatives as Potential Anticancer Agents.Molecules (Basel, Switzerland) · 2024Review
Corrections and comments
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Authors and funding
6 authors.
Funding
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Abstract
Artesunate (ART), an effective antimalarial semisynthetic derivative of artemisinin, exhibits antitumour properties, but the mechanism(s) involved remain elusive. In this study, we investigated the antitumour effects of ART on human oesophageal squamous cell carcinoma (ESCC) cell lines. Treatment of ESCC cell lines with ART resulted in the production of excessive reactive oxygen species (ROS) that induced DNA damage, reduced cell proliferation and inhibited clonogenicity via G1-S cell cycle arrest and/or apoptosis in vitro. The administration of ART to nude mice with ESCC cell xenografts inhibited tumour formation in vivo. However, the cytotoxicity of ART strongly differed among the ESCC cell lines tested. Transcriptomic profiling revealed that although the expression of large numbers of genes in ESCC cell lines was affected by ART treatment, these genes could be functionally clustered into pathways involved in regulating cell cycle progression, DNA metabolism and apoptosis. We revealed that p53 and Cdk4/6-p16-Rb cell cycle checkpoint controls were critical determinants required for mediating ART cytotoxicity in ESCC cell lines. Specifically, KYSE30 cells with p53
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