ArticleNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2015
Dihydroartemisinin suppresses glioma proliferation and invasion via inhibition of the ADAM17 pathway.
Article in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 31 citations in OpenAlex.
- Sesquiterpene Lactones as Promising Anti-Glioblastoma Drug Candidates Exerting Complex Effects on Glioblastoma Cell Viability and Proneural-Mesenchymal Transition.Biomedicines · 2025Review
- ADAM17 Confers Temozolomide Resistance in Human Glioblastoma Cells and miR-145 Regulates Its Expression.International journal of molecular sciences · 2023Article
- Ferroptosis and Its Potential Role in Glioma: From Molecular Mechanisms to Therapeutic Opportunities.Antioxidants (Basel, Switzerland) · 2022Review
- Ferroptosis Involvement in Glioblastoma Treatment.Medicina (Kaunas, Lithuania) · 2022Review
- The multifaceted NF-kB: are there still prospects of its inhibition for clinical intervention in pediatric central nervous system tumors?Cellular and molecular life sciences : CMLS · 2021Review
- Dihydroartemisinin initiates ferroptosis in glioblastoma through GPX4 inhibition.Bioscience reports · 2020Article
- Dihydroartemisinin Induces Growth Arrest and Overcomes Dexamethasone Resistance in Multiple Myeloma.Frontiers in oncology · 2020Article
- A Disintegrin and Metalloproteinase 8 as a Potential Blood Biomarker for Early Diagnosis of Gastric Cancer.Yonsei medical journal · 2019Article
- Antitumor Research on Artemisinin and Its Bioactive Derivatives.Natural products and bioprospecting · 2018Review
- ADAM-17 is a poor prognostic indicator for patients with hilar cholangiocarcinoma and is regulated by FoxM1.BMC cancer · 2018Article
- FoxM1 drives ADAM17/EGFR activation loop to promote mesenchymal transition in glioblastoma.Cell death & disease · 2018Article
- AKT Axis, miR-21, and RECK Play Pivotal Roles in Dihydroartemisinin Killing Malignant Glioma Cells.International journal of molecular sciences · 2017Article
- Article
- Fatal Liver and Bone Marrow Toxicity by Combination Treatment of Dichloroacetate and Artesunate in a Glioblastoma Multiforme Patient: Case Report and Review of the Literature.Frontiers in oncology · 2016Article
- Updates on artemisinin: an insight to mode of actions and strategies for enhanced global production.Protoplasma · 2016Review
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dihydroartemisinin (DHA) is a semi-synthetic derivative of artemisinin, a well-tolerated and effective drug for malaria treatment, and has recently been shown to have antitumorigenic activity. However, the mechanistic basis of these activities in gliomas is unknown. The objective of this study was to evaluate whether DHA inhibits cell proliferation and invasion in glioma cells, and to elucidate the underlying mechanisms. The results demonstrate that DHA treatment significantly inhibited cell proliferation, migration and invasion, as determined using viability, transwell migration, and matrix penetration assays, respectively. Western blot analysis revealed that protein expression levels of a disintegrin and metalloproteinase 17 (ADAM17), and phosphorylated epidermal growth factor receptor and AKT (p-EGFR and p-AKT, respectively), were suppressed by DHA. EGFR and AKT phosphorylation was enhanced by stimulation with the ADAM17 agonist chemokine phorbol myristate acetate. These data suggest that DHA inhibits glioma proliferation and invasion through suppression of ADAM17 and downregulation of EGFR-PI3 K-AKT signaling.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.