ArticleGenes & diseases2026
Targeting Wnt/β-catenin activation in combination with temozolomide leads to glioblastoma inhibition and long-term survival in mice.
Article in Genes & diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 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
- Article
- Antibody therapies in glioblastoma: Overcoming micro-environmental barriers.Iranian journal of basic medical sciences · 2026Review
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Authors and funding
6 authors.
Funding
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Abstract
Glioblastoma (GBM) is one of the most treatment-resistant brain malignancies. Dysregulation of Wnt/β-catenin signaling might be implicated in tumorigenesis of GBM. In this study, spatial transcriptomic analysis revealed elevated expression of Wnt target genes within tumor regions compared with peritumoral tissues. Overexpression of porcupine (PORCN), an O-acyltransferase for Wnt secretion, correlated with poor prognosis of GBM patients. Treatment with Wnt-C59, a PORCN inhibitor, inhibited Wnt signaling, hindered GBM cell proliferation and invasion, and inhibited GBM stem cells' self-renewal properties in a dose-dependent manner. Moreover, using β-catenin knockout and knockdown cells, FOXM1 was identified as a downstream transcription target of Wnt/β-catenin signaling. Wnt-C59 inhibited the expression of FOXM1 in GBM cells. Furthermore, Wnt-C59 demonstrated the ability to impede tumor formation and enhance the overall survival of mice bearing GBM in a preclinical model. Notably, the combined treatment of Wnt-C59 with temozolomide further enhanced therapeutic outcomes, leading to a significant extension of overall survival in GBM-bearing mice. Mechanistically, Wnt-C59 significantly down-regulated the expression of oncogenic targets associated with Wnt/β-catenin signaling (FOXM1, cyclin D, and C-Myc) both
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