Dihydroartemisinin inhibits EphA2/PI3K/Akt pathway-mediated malignant behaviors and vasculogenic mimicry in glioma stem cells
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Huangde Fu1,2, Shengtian Wu1, Hechun Shen1
1Department of Neurosurgery, The Second Nanning People's Hospital, Guangxi, China.
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.
Insights
Dihydroartemisinin (DHA) inhibits glioma progression by targeting EphA2 expression. This study reveals DHA
Area of Science:
- Neuro-oncology
- Molecular Biology
- Cancer Research
Background:
- Gliomas are primary brain tumors with poor prognosis.
- EphA2 is implicated in glioma progression and vasculogenic mimicry (VM).
- Dihydroartemisinin (DHA) shows anti-glioma activity but its EphA2 interaction is unclear.
Purpose of the Study:
- To investigate DHA's effect on EphA2 expression in glioma.
- To elucidate the role of the PI3K/Akt pathway in DHA's anti-glioma mechanisms.
- To assess DHA as a potential therapeutic agent targeting EphA2 and VM.
Main Methods:
- In vitro studies using C6 glioma stem cells.
- Assessment of vasculogenic-like network formation.
- Analysis of EphA2 expression and PI3K/Akt pathway activation.
- In vivo tumor growth studies.
Main Results:
- DHA significantly inhibited glioma stemness, VM, and tumor growth.
- DHA suppressed EphA2 expression, which was linked to its anti-tumor effects.
- The PI3K/Akt pathway was identified as a mediator of DHA's action.
- Overexpression of EphA2 partially reversed DHA's anti-tumor effects.
Conclusions:
- DHA effectively inhibits glioma progression by downregulating EphA2.
- The PI3K/Akt pathway plays a crucial role in mediating DHA's therapeutic effects.
- Targeting EphA2 and VM with DHA presents a promising therapeutic strategy for gliomas.
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