Sunitinib impedes brain tumor progression and reduces tumor-induced neurodegeneration in the microenvironment
Gökçe Hatipoglu1, Stefan W Hock, Ruth Weiss
1Department of Neurosurgery, Universitätsklinikum Erlangen, Friedrich Alexander University Erlangen-Nürnberg (FAU), Erlangen, Germany.
Abstract:
Malignant gliomas can be counted to the most devastating tumors in humans. Novel therapies do not achieve significant prolonged survival rates. The cancer cells have an impact on the surrounding vital tissue and form tumor zones, which make up the tumor microenvironment. We investigated the effects of sunitinib, a small molecule multitargeted receptor tyrosine kinase inhibitor, on constituents of the tumor microenvironment such as gliomas, astrocytes, endothelial cells, and neurons. Sunitinib has a known anti-angiogenic effect. We found that sunitinib normalizes the aberrant tumor-derived vasculature and reduces tumor vessel pathologies (i.e. auto-loops). Sunitinib has only minor effects on the normal, physiological, non-proliferating vasculature. We found that neurons and astrocytes are protected by sunitinib against glutamate-induced cell death, whereas sunitinib acts as a toxin towards proliferating endothelial cells and tumor vessels. Moreover, sunitinib is effective in inducing glioma cell death. We determined the underlying pathways by which sunitinib operates as a toxin on gliomas and found vascular endothelial growth factor receptor 2 (VEGFR2, KDR/Flk1) as the main target to execute gliomatoxicity. The apoptosis-inducing effect of sunitinib can be mimicked by inhibition of VEGFR2. Knockdown of VEGFR2 can, in part, foster the resistance of glioma cells to receptor tyrosine kinase inhibitors. Furthermore, sunitinib alleviates tumor-induced neurodegeneration. Hence, we tested whether temozolomide treatment could be potentiated by sunitinib application. Here we show that sunitinib can amplify the effects of temozolomide in glioma cells. Thus, our data indicate that combined treatment with temozolomide does not abrogate the effects of sunitinib. In conclusion, we found that sunitinib acts as a gliomatoxic agent and at the same time carries out neuroprotective effects, reducing tumor-induced neurodegeneration. Thus, this report uncovered sunitinib's actions on the brain tumor microenvironment, revealing novel aspects for adjuvant approaches and new clinical assessment criteria when applied to brain tumor patients.
Insights
Sunitinib, a targeted therapy, kills malignant glioma cells by inhibiting vascular endothelial growth factor receptor 2 (VEGFR2) and protects neurons. It also enhances temozolomide treatment efficacy for brain tumors.
Area of Science:
- Oncology
- Neuroscience
- Pharmacology
Background:
- Malignant gliomas are aggressive brain tumors with limited treatment options.
- The tumor microenvironment significantly influences glioma progression and treatment resistance.
- Novel therapeutic strategies targeting the tumor microenvironment are urgently needed.
Purpose of the Study:
- To investigate the effects of sunitinib, a multi-targeted receptor tyrosine kinase inhibitor, on malignant gliomas and their microenvironment.
- To elucidate the mechanisms underlying sunitinib's action on glioma cells, endothelial cells, neurons, and astrocytes.
- To evaluate the potential of sunitinib as an adjuvant therapy in combination with temozolomide.
Main Methods:
- In vitro studies on glioma cells, endothelial cells, astrocytes, and neurons.
- Assessment of sunitinib's effects on tumor vasculature and cell viability.
- Investigation of molecular pathways, including vascular endothelial growth factor receptor 2 (VEGFR2) inhibition.
- Combination treatment studies with temozolomide.
Main Results:
- Sunitinib normalizes aberrant tumor vasculature and reduces vessel pathologies.
- Sunitinib exhibits direct toxicity towards proliferating endothelial cells and glioma cells, primarily through VEGFR2 inhibition.
- Sunitinib protects neurons and astrocytes from glutamate-induced cell death and alleviates neurodegeneration.
- Sunitinib potentiates the anti-glioma effects of temozolomide.
Conclusions:
- Sunitinib demonstrates dual action as a gliomatoxic agent and a neuroprotective compound.
- Targeting VEGFR2 is crucial for sunitinib's efficacy against gliomas.
- Sunitinib holds promise as an adjuvant therapy to enhance temozolomide treatment for malignant gliomas.
- Understanding sunitinib's impact on the brain tumor microenvironment offers new avenues for clinical applications.
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