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Artesunate Inhibits the Growth of Insulinoma Cells via SLC7A11/ GPX4-mediated Ferroptosis
Fengping Chen1, Jiexia Lu1, Biaolin Zheng1,2
1Department of Gastroenterology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China.
Background:
Artesunate (ART) has been recognized to induce ferroptosis in various tumor phenotypes, including neuroendocrine tumors. We aimed to investigate the effects of ART on insulinoma and the underlying mechanisms by focusing on the process of ferroptosis.
Methods:
The CCK8 and colony formation assays were conducted to assess the effectiveness of ART. Lipid peroxidation, glutathione, and intracellular iron content were determined to validate the process of ferroptosis, while ferrostatin-1 (Fer-1) was employed as the inhibitor of ferroptosis. Subcutaneous tumor models were established and treated with ART. The ferroptosis-associated proteins were determined by western blot and immunohistochemistry assays. Pathological structures of the liver were examined by hematoxylin-eosin staining.
Results:
ART suppressed the growth of insulinoma both in vitro and in vivo. Insulinoma cells treated by ART revealed signs of ferroptosis, including increased lipid peroxidation, diminished glutathione levels, and ascending intracellular iron. Notably, ART-treated insulinoma cells exhibited a decline in the expressions of catalytic component solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4). These alterations were negated by Fer-1. Moreover, no hepatotoxicity was observed upon the therapeutic dose of ART.
Conclusion:
Artesunate might regulate ferroptosis of insulinoma cells through the SLC7A11/GPX4 pathway.
Insights
Artesunate (ART) effectively inhibits insulinoma growth by inducing ferroptosis, a cell death process. This occurs via the SLC7A11/GPX4 pathway, with no observed liver toxicity.
Area of Science:
- Oncology
- Cell Death Mechanisms
- Pharmacology
Background:
- Artesunate (ART) is known to induce ferroptosis in various cancer types.
- Neuroendocrine tumors, including insulinoma, are potential targets for ferroptosis-inducing agents.
- The specific effects of ART on insulinoma and its ferroptosis-related mechanisms require elucidation.
Purpose of the Study:
- To investigate the anti-tumor effects of Artesunate (ART) on insulinoma.
- To explore the underlying mechanisms of ART-induced ferroptosis in insulinoma cells.
- To assess the safety profile of ART in the context of insulinoma treatment.
Main Methods:
- Cell viability and proliferation assays (CCK8, colony formation) were used to evaluate ART's efficacy.
- Ferroptosis was validated by measuring lipid peroxidation, glutathione, and intracellular iron levels.
- In vivo tumor models and western blot/immunohistochemistry were employed to analyze ferroptosis-associated proteins (SLC7A11, GPX4).
Main Results:
- Artesunate significantly suppressed insulinoma growth both in vitro and in vivo.
- ART induced hallmarks of ferroptosis in insulinoma cells, including increased lipid peroxidation and iron, and decreased glutathione.
- ART treatment led to reduced expression of SLC7A11 and GPX4, key regulators of ferroptosis, an effect reversed by the ferroptosis inhibitor Fer-1. No hepatotoxicity was detected.
Conclusions:
- Artesunate demonstrates potent anti-insulinoma activity by inducing ferroptosis.
- The SLC7A11/GPX4 pathway is implicated in ART-mediated ferroptosis in insulinoma.
- Artesunate presents a potential therapeutic strategy for insulinoma with a favorable safety profile.
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