ArticleCancer medicine2026
C1orf226 Promotes Glioma Stemness and Oncogenesis in Glioma via PLK1-Mediated Wnt/β-Catenin Signaling.
Article in Cancer medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
introductionGlioma stem cells (GSCs) are pivotal drivers of tumor progression and therapeutic resistance; however, the underlying regulatory mechanisms have not been fully elucidated. This study aimed to identify novel oncogenic drivers in glioma via a comprehensive multiomics analysis.
methodsWe integrated three datasets to screen potential oncogenic drivers. Functional experiments were performed to examine the effects of C1orf226 on glioma cell proliferation, cell cycle, epithelial-mesenchymal transition (EMT), and apoptosis. Additionally, tumor sphere formation assays, ALDH+/CD133+ cell detection, and stemness marker analysis were used to evaluate the role of C1orf226 in GSC stemness. Mechanistic studies involving immunoprecipitation (IP) and ubiquitination assays were applied to characterize the interaction between C1orf226 and PLK1, as well as their regulation on β-catenin stability and Wnt/β-catenin signaling. Rescue assays further verified the functional crosstalk between C1orf226 and PLK1. Xenograft mouse models were used in vivo to assess the impacts of C1orf226 knockdown on tumor growth and stemness markers.
resultsC1orf226 was significantly upregulated in glioma tissues compared with normal brain tissues. Its high expression correlated with shorter patient survival and served as an independent prognostic factor in the CGGA cohort. In vitro, C1orf226 exerted oncogenic function by facilitating cell proliferation, cell cycle progression, EMT-like processes, and stemness, and suppressing apoptosis. Mechanistically, C1orf226 interacts with PLK1 to block its degradation, thereby activating PLK1 and downstream Wnt/β-catenin signaling. Rescue experiments verified that PLK1 overexpression restored β-catenin stability, Wnt/β-catenin target gene expression, and GSC properties impaired by C1orf226 knockdown. In vivo, C1orf226 knockdown restrained xenograft growth and reduced stemness marker levels, and PLK1 co-expression abrogated these effects.
conclusionsOur findings reveal that C1orf226 is a PLK1-dependent regulator of Wnt/β-catenin signaling and GSC plasticity, highlighting its potential as a promising therapeutic target in glioma.
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