ArticleThe Kaohsiung journal of medical sciences2023
Dihydroartemisinin enhances gefitinib cytotoxicity against lung adenocarcinoma cells by inducing ROS-dependent apoptosis and ferroptosis.
Article in The Kaohsiung journal of medical sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 27 citations in OpenAlex.
- Nano-hydrogel-based delivery system for dihydroartemisinin to enhance cuproptosis and synergize with anti-PD-1 therapy in triple-negative breast cancer.Journal of nanobiotechnology · 2026Article
- Establishment and validation of an ADP-ribosylation-related gene signature for prognostic prediction in lung adenocarcinoma.Discover oncology · 2026Article
- Research Progress on Chinese Herbal Medicine Components Targeting Ferroptosis for Cancer Therapy.Molecules (Basel, Switzerland) · 2026Review
- The Therapeutic Potential of Dihydroartemisinin in Cancer Treatment.International journal of molecular sciences · 2026Review
- Natural compounds for non-small cell lung cancer treatment: focus on the EGFR signaling pathway.Frontiers in pharmacology · 2026Review
- Lipid reprogramming and ferroptosis crosstalk in clear cell renal cell carcinoma: metabolic vulnerabilities and therapeutic targeting.Molecular cancer · 2025Review
- The inhibitory effect of M2 macrophage-derived exosomes on gefitinib resistant lung adenocarcinoma cells through the MIF/TIMP1/CD74 axis.Scientific reports · 2025Article
- Ferroptosis in cancer: revealing the multifaceted functions of mitochondria.Cellular and molecular life sciences : CMLS · 2025Review
- Artemisiae Annuae Herba: from anti-malarial legacy to emerging anti-cancer potential.Theranostics · 2025Review
- Artemisinin and its derivatives: all-rounders that may prevent the progression from lung injury to lung cancer.Frontiers in pharmacology · 2025Review
- Dual role of autophagy in bone metastasis: mechanistic insights and therapeutic targeting.American journal of clinical and experimental urology · 2025Review
- Dihydroartemisinin targets the miR-497-5p/SOX5 axis to suppress tumor progression in non-small cell lung cancer.Frontiers in pharmacology · 2025Article
- [Role of Mitochondria in Ferroptosis and Its Relationship to Tumors].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2024Review
- FTO/m6A mediates miR-138-5p maturation and regulates gefitinib resistance of lung adenocarcinoma cells by miR-138-5p/LCN2 axis.BMC cancer · 2024Article
- Natural products targeting ferroptosis pathways in cancer therapy (Review).Oncology reports · 2024Review
- Dihydroartemisinin restores the immunogenicity and enhances the anticancer immunosurveillance of cisplatin by activating the PERK/eIF2α pathway.Cell & bioscience · 2024Article
- Review
- Promoting reactive oxygen species accumulation to overcome tyrosine kinase inhibitor resistance in cancer.Cancer cell international · 2024Review
- Blockage of Autophagy for Cancer Therapy: A Comprehensive Review.International journal of molecular sciences · 2024Review
- [Role of Ferroptosis in Non-small Cell Lung Cancer and Progress of Traditional Chinese Medicine Intervention].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2024Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The application of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), such as gefitinib, has shifted lung cancer treatment from empirical chemotherapy to targeted molecular therapy. However, acquired drug resistance is inevitable in almost all non-small cell lung cancer (NSCLC) patients treated with gefitinib. Combined treatment with dihydroartemisinin (DHA) and gefitinib produced a better inhibitory effect on lung adenocarcinoma than gefitinib treatment alone; however, the specific mechanism remains unclear. In this study, we aimed to assess the underlying mechanism of this combination treatment. We prepared gefitinib-resistant A549 cells and investigated whether apoptosis and ferroptosis were involved in the sensitizing effect of DHA. Treatment with 5 μM gefitinib resulted in rupturing and floatation of A549 cells in the medium, while A549-GR cells were found to be insusceptible to gefitinib. However, treatment with DHA substantially inhibited the proliferation of A549-GR cells in a dose-dependent manner accompanied by increased apoptosis and ferroptosis. The accumulated reactive oxygen species (ROS) was crucial for the inhibitory effect of DHA on A549-GR cells. Moreover, cellular autophagy was significantly upregulated post-DHA treatment. The combined treatment of DHA and gefitinib resulted in inhibition of proliferation of A549, H1975, and HCC827 cells, and ROS accumulation and a remarkable induction of apoptosis was observed in A549-GR cells. DHA significantly induced apoptosis and ferroptosis in a dose-dependent manner and exhibited high cellular toxicity on A549-GR cells when combined with gefitinib.
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