ArticleCell death & disease2025
Atypical cadherin CELSR2 acts as a therapeutic target for glioma through WNT3A/β-catenin signaling.
Article in Cell death & disease, 2025. 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.
- Carbohydrate responsive element binding protein promotes colorectal carcinogenesis via Wnt/β-catenin pathway.Oncogene · 2026Article
- Causal statistical association between remnant cholesterol and coronary heart disease: genetic insights into the PSRC1-CELSR2-SORT1 gene cluster.Journal of lipid research · 2026Article
- Therapeutic targeting of adhesion GPCRs: a status update and future potential.Expert opinion on drug discovery · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Glioma is the most common primary brain tumors and has a high recurrence and mortality rate after surgery. Most gliomas are of astrocytic origin. We recently demonstrated that Celsr2 is essential for injury-induced responses and functions of astrocytes, while its role in the development and treatment of gliomas remains unexplored. In this study, an increase of CELSR2 expression was identified in patient glioma samples and glioma cell lines, and higher levels of CELSR2 correlate with poorer patient survival as indicated by TCGA data. In cultured glioma cells, CELSR2 knockdown reduced proliferation and caused cell cycle arrest, which was further supported by proteomic analysis. CELSR2 knockdown inhibited Wnt/β-catenin signaling, and the effect could be reversed by activating β-catenin using GSK-3β inhibitor in glioma cells. WNT3A efficiently enhanced the proliferation of glioma cells and activated the downstream signaling, which were significantly compromised by CELSR2 knockdown. We developed magnetic nanoparticles loaded with CELSR2-siRNA, which suppressed tumor growth in glioma-inoculated nude mice. In conclusion, CELSR2 positively regulates glioma development through WNT3A/β-catenin signaling and inhibiting CESLR2 is a novel therapeutic strategy for gliomas.
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