ArticleOncogene2025
GNAO1 overexpression promotes neural differentiation of glioma stem-like cells and reduces tumorigenicity through TRIM21/CREB/HES1 axis.
Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- TRIM21 inhibition alleviates acute kidney injury by promoting INTS3-associated DNA damage repair.Apoptosis : an international journal on programmed cell death · 2026Article
- Novel MAFG-METTL14-SCD1 axis regulates lipid metabolism mediating choroidal melanoma distant metastasis.Journal of experimental & clinical cancer research : CR · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Inducing tumor cell differentiation is a promising strategy for treating malignant cancers, including glioma, yet the critical regulator(s) underlying glioma cell differentiation is poorly understood. Here, we identify G Protein Subunit Alpha O1 (GNAO1) as a critical regulator of neural differentiation of glioma stem-like cells (GSCs). GNAO1 expression was lower in gliomas than in normal neuronal tissues and high expression of GNAO1 correlated with a better prognosis. GNAO1 overexpression markedly promoted neural differentiation of GSCs, leading to decreased cell proliferation and colony formation. Mechanistically, GNAO1 recruited TRIM21 and facilitated TRIM21-mediated ubiquitination. This ubiquitination resulted in the degradation of CREB and further reduced p300-mediated H3K27ac levels of the HES1 promoter. As a result, GNAO1 overexpression downregulated HES1 expression, which reinforced neuronal differentiation. In addition, knockdown of METTL3, a key writer of the N
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Registered trials
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