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β-Mangostin targets and suppresses glioma via STING activation and tumor-associated microglia polarization
Yimin Yang1, Xuling Luo1, Yaling Wang2
1College of Pharmaceutical Sciences, Zhejiang University of Technology, Hangzhou, Zhejiang 310014, China.
Abstract:
Glioma, a common and highly malignant central nervous system tumor, markedly influences patient prognosis via interactions with glioma-associated macrophages. Previous research has revealed the anticancer potential of β-mangostin, a xanthone derivative obtained from the mangosteen fruit. This research investigated the role of β-mangostin on microglia in the glioma microenvironment and evaluated the efficacy of β-mangostin combined with anti-PD-1 antibody (αPD-1) in glioma-bearing mice. The results showed that, β-mangostin attenuated M2 polarization in BV2 cells and promoted M1-related interleukin (IL)-1β and IL-6 secretion, thereby inhibiting glioma invasion. In addition, β-mangostin improved the anti-glioma effects of αPD-1 and increased CD8+T cell and M1-type microglia infiltration. Mechanistically, β-mangostin bound to the stimulator of interferon genes (STING) protein, which is crucial for the anti-tumor innate immune response, and promoted STING phosphorylation in microglia, both in vivo and in vitro. These results provide insights into its mode of action and supporting further investigation into β-mangostin as a therapeutic agent.
Insights
Beta-mangostin, derived from mangosteen, shows promise in treating glioma by reprogramming microglia and enhancing anti-PD-1 therapy. This compound targets the STING pathway to boost anti-tumor immunity.
Area of Science:
- Immunology
- Neuro-oncology
- Pharmacology
Background:
- Glioma is a malignant brain tumor influenced by glioma-associated macrophages.
- Beta-mangostin, a mangosteen derivative, exhibits anticancer properties.
- Microglia play a key role in the glioma microenvironment.
Purpose of the Study:
- To investigate beta-mangostin's effect on microglia in glioma.
- To evaluate the combination therapy of beta-mangostin and anti-PD-1 (αPD-1) in glioma models.
- To elucidate the molecular mechanism of beta-mangostin's action.
Main Methods:
- In vitro studies using BV2 cells to assess M2/M1 polarization and cytokine secretion.
- In vivo experiments with glioma-bearing mice treated with beta-mangostin and αPD-1.
- Analysis of immune cell infiltration (CD8+ T cells, M1 microglia).
- Investigation of beta-mangostin's interaction with the STING pathway via phosphorylation assays.
Main Results:
- Beta-mangostin inhibited M2 polarization and promoted M1 polarization in microglia, increasing IL-1β and IL-6 secretion.
- Beta-mangostin enhanced the efficacy of αPD-1 therapy against glioma.
- The combination therapy increased CD8+ T cell and M1 microglia infiltration in the tumor microenvironment.
- Beta-mangostin directly bound to and promoted the phosphorylation of STING in microglia.
Conclusions:
- Beta-mangostin modulates microglia polarization and enhances anti-glioma immune responses.
- Combination of beta-mangostin with αPD-1 shows synergistic therapeutic potential.
- Beta-mangostin acts via the STING pathway in microglia to mediate its anti-tumor effects.
- Beta-mangostin is a potential therapeutic agent for glioma treatment.
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