ArticleFrontiers in oncology2014
Dihydroartemisinin is a Hypoxia-Active Anti-Cancer Drug in Colorectal Carcinoma Cells.
Article in Frontiers in oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Initial Evaluation of Dihydroartemisinin (DHA), Metformin and Taro Extract in Combination with Cisplatin for Enhanced Cytotoxicity in Triple-Negative Breast Cancer (TNBC) Cell Lines.Journal of analytical oncology · 2026Article
- Hypofractionated radiotherapy (RT) combined with dihydroartemisinin (DHA): No synergistic effect observed in a preliminary animal study.Precision radiation oncology · 2025Article
- Research Progress on Stimulus-Responsive Polymer Nanocarriers for Cancer Treatment.Pharmaceutics · 2023Review
- Co-delivery of dihydroartemisinin and pyropheophorbide-iron elicits ferroptosis to potentiate cancer immunotherapy.Biomaterials · 2022Article
- Dihydroartemisinin is potential therapeutics for treating late-stage CRC by targeting the elevated c-Myc level.Cell death & disease · 2021Article
- Dihydroartemisinin and its anticancer activity against endometrial carcinoma and cervical cancer: involvement of apoptosis, autophagy and transferrin receptor.Singapore medical journal · 2021Article
- Dihydroartemisinin inhibits activation of the AIM2 inflammasome pathway and NF-κB/HIF-1α/VEGF pathway by inducing autophagy in A431 human cutaneous squamous cell carcinoma cells.International journal of medical sciences · 2021Article
- Advanced Computational Methodologies Used in the Discovery of New Natural Anticancer Compounds.Frontiers in pharmacology · 2021Review
- Dihydroartemisinin inhibits HepG2.2.15 proliferation by inducing cellular senescence and autophagy.BMB reports · 2019Article
- Dihydroartemisinin Protects against Dextran Sulfate Sodium-Induced Colitis in Mice through Inhibiting the PI3K/AKT and NF-BioMed research international · 2019Article
- Codelivery of dihydroartemisinin and doxorubicin in mannosylated liposomes for drug-resistant colon cancer therapy.Acta pharmacologica Sinica · 2017Article
- Dihydroartemisinin Exerts Anti-Tumor Activity by Inducing Mitochondrion and Endoplasmic Reticulum Apoptosis and Autophagic Cell Death in Human Glioblastoma Cells.Frontiers in cellular neuroscience · 2017Article
- [Progress on anti-tumor molecular mechanisms of dihydroartemisinin].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2016Article
- The molecular and cellular action properties of artemisinins: what has yeast told us?Microbial cell (Graz, Austria) · 2016Review
- Deubiquitylating enzyme USP9x regulates radiosensitivity in glioblastoma cells by Mcl-1-dependent and -independent mechanisms.Cell death & disease · 2016Article
- Dihydroartemisinin increases temozolomide efficacy in glioma cells by inducing autophagy.Oncology letters · 2015Article
- Cellular stress responses in cancer and cancer therapy.Frontiers in oncology · 2014Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor hypoxia is one main biological factor that drives resistance to chemotherapy and radiotherapy. To develop a novel strategy for overcoming hypoxia-induced therapy resistance, we examined the anti-neoplastic activity of the reactive oxygen donor dihydroartemisinin (DHA) in human colon cancer cell lines in normoxia and severe hypoxia. In addition, we analyzed the involvement of the intrinsic apoptosis pathway for DHA-mediated cytotoxicity in HCT116 cells in short-term and long-term in vitro assays. When applied at lower concentrations (≤25 μM), DHA induced apoptosis in Colo205, HCT15, and HCT116 cells, whereas necrotic cell death was increased when cells were treated with higher DHA concentrations (50 μM). However, no preference for DHA-induced apoptosis or necrosis could be detected between the treatment under normoxic or hypoxic conditions. Moreover, DHA potently reduced clonogenic survival of HCT116 cells in normoxia and hypoxia. Treatment of HCT116 cells with 25 μM DHA resulted in activation of Bax under normoxic and hypoxic conditions. Interestingly, cytochrome c release from the mitochondria and caspase-activation were observed only under normoxic conditions, whereas, under hypoxic conditions DHA induced a caspase-independent apoptosis-like cell death. However, under both conditions, generation of reactive oxygen species was an important mediator of DHA-induced toxicity. Further molecular analysis suggests that DHA-mediated cell death involves different sets of pro-apoptotic Bcl-2 family members. The pronounced cytotoxic activity of DHA in severe hypoxia as well as normoxia offers new perspectives for targeting the hypoxic tumor cell fraction to improve treatment outcome for cancer patients.
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