ArticleJCI insight2025
The AURKA inhibitor alters the immune microenvironment and enhances targeting B7-H3 immunotherapy in glioblastoma.
Article in JCI insight, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Investigating the prognostics and theranostic cell cycle-related genes of Hinokinin in high-grade glioma: an integrated network pharmacology, bioinformatics, and molecular docking approach.Journal, genetic engineering & biotechnology · 2026Article
- Igniting cold tumors: reprogramming the tumor immune microenvironment with dual-payload ADCs in combination with PD-L1&4-1BB bispecific antibodies.Journal for immunotherapy of cancer · 2026Article
- Low-affinity binding of anti-B7-H3 clone MJ18 to murine B7-H3 fails to induce tumor regression.Scientific reports · 2026Article
- The Search for Predictive Biomarkers in Response to Immune Checkpoint Inhibitors and Associated Adverse Events.Journal of personalized medicine · 2025Review
- Aurora kinase-a expression heterogeneity and potential benefit of combination therapy in prostate adenocarcinoma.Frontiers in cell and developmental biology · 2025Article
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Authors and funding
17 authors.
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Abstract
Glioblastoma (GBM) is one of the most lethal adult brain tumors with limited effective therapeutic options. Immunotherapy targeting B7-H3 (CD276) has shown promising efficacy in the treatment of gliomas. However, the response to this treatment varies among glioma patients due to individual differences. It's necessary to find an effective strategy to improve the efficacy of targeting B7-H3 immunotherapy for nonresponders. In this study, we demonstrated a strong correlation between aurora kinase A (AURKA) and CD276 expression in glioma tissue samples. Additionally, both AURKA knockdown and overexpression resulted in parallel changes in B7-H3 expression levels in glioma cells. Mechanistically, AURKA elevated B7-H3 expression by promoting epidermal growth factor receptor (EGFR) phosphorylation, which was validated in glioma cell lines and primary GBM cells. What's more, the combination of AURKA inhibitor (alisertib) and anti-B7-H3 antibody markedly reduced tumor size and promoted CD8+ T cell infiltration and activation in mouse orthotopic syngeneic glioma models. To our knowledge, this study is the first to demonstrate AURKA-mediated B7-H3 upregulation in glioma cells; moreover, it proposes a promising therapeutic strategy combining the AURKA inhibitor alisertib with B7-H3-specific blocking mAbs.
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