ArticleHeliyon2025
Dihydroartemisinin inhibits EphA2/PI3K/Akt pathway-mediated malignant behaviors and vasculogenic mimicry in glioma stem cells.
Article in Heliyon, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Dihydroartemisinin Suppresses Hepatocellular Carcinoma Progression by Acting on KIF11 with PI3K/Akt Modulation.Cancers · 2026Article
- The Therapeutic Potential of Dihydroartemisinin in Cancer Treatment.International journal of molecular sciences · 2026Review
- Therapeutic profiling of dihydroartemisinin using in vitro and in vivo models reveals anti-glioma potential.Cancer cell international · 2026Article
- Apolipoprotein E (APOE) Promotes Cell Proliferation and Invasion in Glioma via the PI3K/AKT Signaling Pathway.Cancer management and research · 2026Article
- The Roles of RNA-Binding Proteins in Vasculogenic Mimicry Regulation in Glioblastoma.International journal of molecular sciences · 2025Review
- Zmynd11 is essential for neurogenesis by coordinating H3K36me3 modification of Epha2 and PI3K signaling pathway.Cell & bioscience · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gliomas, the most prevalent primary brain tumors, exhibit a poor five-year survival rate despite advances in various treatments, necessitating further studies to understand tumor progression and develop new therapies, particularly targeting EphA2, which is implicated in vasculogenic mimicry and glioma progression. Dihydroartemisinin (DHA) has shown anti-glioma effects through mechanisms such as PERK-related ferroptosis and inhibition of proliferation and angiogenesis, although its interaction with EphA2 in mediating these effects requires further investigation. In this study, we revealed that DHA significantly inhibits the formation of vasculogenic-like networks, the stemness of C6 glioma stem cells and the growth of glioma by inhibiting the expression of EphA2. Mechanistic investigations indicated that PI3K/Akt pathway at least partly mediated this function, since overexpression of EphA2 reversed the anti-tumor effects of DHA. Conclusively, the current report provides evidence that DHA, PI3K/Akt/EphA2 blockage, and VM inhibition are promising therapies for glioma.
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Registered trials
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