Abstract
Glioma, marked by a low mutational burden, low immunogenicity, high heterogeneity, and the challenges posed by the blood-brain barrier, continues to be a major hurdle in neuro-oncology. Current research underscores the necessity for more effective medications and treatment strategies. In this study, we explored the role of Apolipoprotein E (ApoE) in glioma using both bioinformatics and experimental methods. The construction of our bioinformatics risk model identified ApoE as a protective factor linked to longer survival in glioma patients. Subsequently, we created an in situ tumorigenic mouse model and a subcutaneous tumorigenic mouse model with ApoE gene knockout to evaluate the functional impacts of ApoE deficiency in glioma. Our results demonstrated that ApoE deficiency accelerates the growth of glioma and encourages the invasive behaviour of tumour cells into normal brain tissue. Additionally, we detected a reduction in the immune surveillance of glioma in the context of ApoE deficiency. Furthermore, flow cytometry analysis indicated that the lack of ApoE led to a decrease in positive immune cells and an increase in immunosuppressive cells within the tumour microenvironment. Our findings suggest that ApoE plays a crucial role in modulating glioma progression and immune surveillance, highlighting its potential as a therapeutic target.