ArticleCancer immunology, immunotherapy : CII2025
Clofazimine enhances anti-PD-1 immunotherapy in glioblastoma by inhibiting Wnt6 signaling and modulating the tumor immune microenvironment.
Article in Cancer immunology, immunotherapy : CII, 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.
- Systems biology of Wnt signaling in glioma chemotherapy resistance: Integrating multi-omics mechanisms and emerging therapeutic vulnerabilities (Review).Oncology letters · 2026Review
- Astragalus Polysaccharides Target the Wnt/β-catenin Pathway to Suppress Malignant Behavior in Hepatocellular Carcinoma.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2026Article
- WNT signaling in cancer: molecular mechanisms and potential therapies.Molecular biomedicine · 2025Review
- Current strategies and novel immunotherapeutic approaches for overcoming immune resistance in glioblastoma.Discover oncology · 2025Review
- Anti-CD19 CAR T-cell therapy for primary and secondary CNS lymphomas.Bone marrow transplantation · 2025Review
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Glioblastoma multiforme (GBM) is an aggressive and lethal primary brain tumor with limitedtreatment options due to its resistance to conventional therapies and an immunosuppressive tumor microenvironment. In this study, we investigated whether clofazimine, an inhibitor of the Wnt/β-catenin signaling pathway, could enhance the efficacy of anti-PD-1 immunotherapy in GBM. Our in vitro and in vivo experiments demonstrated that clofazimine suppressed GBM cell proliferation, induced apoptosis, and inhibited invasion by downregulating Wnt6-mediated activation of the Wnt/β-catenin pathway and the downstream MEK/ERK signaling cascade, leading to decreased PD-L1 expression. Notably, the combination of clofazimine and anti-PD-1 therapy significantly reduced tumor growth and intracranial invasion in orthotopic GBM mouse models, resulting in extended survival. This combination therapy also reshaped the tumor immune microenvironment by increasing cytotoxic CD8
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Registered trials
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