Wang Cheng, Fan Yiqi, Zhang Lu, Zhao Zhanyi, Luo Feiyang, Sun Kaijian, Zeng Meiqin, Tian Hao, Peng Meichang, Luo Yunhao, Zhao Hailin, He Shuai, Sun Haitao
Neurosurgery Center, The National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China on Diagnosis and Treatment of Cerebrovascular Disease, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, The Neurosurgery Institute of Guangdong Province, Zhujiang Hospital Institute for Brain Science and Intelligence, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Clinical Biobank Center, Microbiome Medicine Center, Guangdong Provincial Clinical Research Center for Laboratory Medicine, Department of Laboratory Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Neurooncol Adv. 2025 Apr 25;7(1):vdaf085. doi: 10.1093/noajnl/vdaf085. eCollection 2025 Jan-Dec.
Recent studies have revealed associations between gut microbiota and glioma. However, the underlying mechanisms remain poorly understood. This study primarily aims to elucidate the impact of altered gut microbiota on tumor progression in glioma-bearing mice.
Fecal samples were collected from glioma patients and healthy controls to compare the effects of human-derived gut microbiota on glioma development in mice. We also analyzed the associations between these microbiota profiles and plasma metabolites.
Significant differences were observed in both the composition and diversity of the gut microbiota between glioma patients and healthy controls. Mice transplanted with gut microbiota from high-grade glioma patients (HGG-FMT) exhibited accelerated glioma progression compared to those transplanted with microbiota from healthy individuals (HC-FMT). Specifically, , , and were significantly enriched in HGG-FMT mice, while and increased in HC-FMT mice. Furthermore, showed a positive correlation with sphingosine, sphingosine 1-phosphate, and D-sphingosine in HGG-FMT mice. Conversely, was positively correlated with stearidonic acid and eicosapentaenoic acid in HC-FMT mice.
Our findings demonstrate that gut microbiota from high-grade glioma patients can promote glioma progression in mice, potentially through mechanisms involving sphingosine 1-phosphate. This metabolite may enter the bloodstream and accelerate glioma growth, offering novel insights into glioma pathogenesis and potential treatment options.
最近的研究揭示了肠道微生物群与胶质瘤之间的关联。然而，其潜在机制仍知之甚少。本研究主要旨在阐明肠道微生物群改变对荷胶质瘤小鼠肿瘤进展的影响。
收集胶质瘤患者和健康对照的粪便样本，以比较人源肠道微生物群对小鼠胶质瘤发展的影响。我们还分析了这些微生物群谱与血浆代谢物之间的关联。
胶质瘤患者和健康对照之间在肠道微生物群的组成和多样性方面均观察到显著差异。与移植健康个体微生物群的小鼠（HC-FMT）相比，移植高级别胶质瘤患者肠道微生物群的小鼠（HGG-FMT）表现出胶质瘤进展加速。具体而言， 、 和 在HGG-FMT小鼠中显著富集，而 和 在HC-FMT小鼠中增加。此外， 在HGG-FMT小鼠中与鞘氨醇、鞘氨醇-1-磷酸和D-鞘氨醇呈正相关。相反， 在HC-FMT小鼠中与十八碳四烯酸和二十碳五烯酸呈正相关。
我们的研究结果表明，高级别胶质瘤患者的肠道微生物群可促进小鼠胶质瘤进展，可能是通过涉及鞘氨醇-1-磷酸的机制。这种代谢物可能进入血液并加速胶质瘤生长，为胶质瘤发病机制和潜在治疗选择提供了新的见解。
