Neuroscience · 2026
Histone acetyltransferase HAT1 drives malignant progression in lower-grade glioma: reshaping the immune microenvironment and molecular mechanisms.
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Sha Zhi, Zhang Zongye, Liu Han, Hou Zhenxing, Wang Dongdong, Zhang Zhichang, Gao Yanzheng, Liu Zhendong
Аннотация
BACKGROUND: HAT1's role in lower-grade glioma (LGG) malignancy and mechanisms is unclear.
METHODS: Multi-omics analysis (TCGA/CGGA transcriptomics, single-cell/spatial transcriptomics, IHC/RT-qPCR) of 906 LGG patients assessed HAT1 expression, prognosis, pathways, immune infiltration, and cellular localization. Molecular docking screened HAT1-targeting drugs.
RESULTS: HAT1 was significantly upregulated in LGG vs. normal brain, correlating with IDH-wildtype status, recurrence, and worse overall survival (independent risk factor). It specifically enriched malignant cell regions. HAT1 overexpression activated cell cycle, adherens junctions, and RIG-I-like signaling. It promoted immune cell infiltration and checkpoint expression. Top FDA-approved compounds with strong binding affinity were identified.
CONCLUSIONS: HAT1 drives LGG malignancy by remodeling the immune microenvironment and activating key oncogenic pathways. Its spatial enrichment in malignant niches and druggability provide a novel basis for targeted-immunotherapy combinations.
METHODS: Multi-omics analysis (TCGA/CGGA transcriptomics, single-cell/spatial transcriptomics, IHC/RT-qPCR) of 906 LGG patients assessed HAT1 expression, prognosis, pathways, immune infiltration, and cellular localization. Molecular docking screened HAT1-targeting drugs.
RESULTS: HAT1 was significantly upregulated in LGG vs. normal brain, correlating with IDH-wildtype status, recurrence, and worse overall survival (independent risk factor). It specifically enriched malignant cell regions. HAT1 overexpression activated cell cycle, adherens junctions, and RIG-I-like signaling. It promoted immune cell infiltration and checkpoint expression. Top FDA-approved compounds with strong binding affinity were identified.
CONCLUSIONS: HAT1 drives LGG malignancy by remodeling the immune microenvironment and activating key oncogenic pathways. Its spatial enrichment in malignant niches and druggability provide a novel basis for targeted-immunotherapy combinations.