ArticleScientific reports2025
ATXN3 deubiquitinates ZEB1 and facilitates epithelial-mesenchymal transition in glioblastoma.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Pharmacological Ascorbate Restrains Epithelial-Mesenchymal Transition and Invasion in Glioblastoma Cells via Extracellular HInternational journal of molecular sciences · 2026Article
- Proton Irradiation Induces Differential Cellular Responses and Proteomic Signatures in Chondrosarcoma and Chondrocytes.Current issues in molecular biology · 2026Article
- Polyglutamine-Expanded Ataxin-3 Accelerates CFTR Degradation Through K63-Linked Ubiquitination to Exacerbate Microglial Inflammation.ASN neuro · 2026Article
- Longikaurin A - Mediated Regulation of ROS/JNK Signaling Counteracts Epithelial-Mesenchymal Transition in Glioblastoma.Neuromolecular medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
The activation of epithelial-mesenchymal transition (EMT) promotes glioblastoma (GBM) invasion, thereby enhancing its malignancy. Elucidating the underlying mechanisms that regulate EMT is essential for the development of effective treatments for GBM. In this study, we found that GBM tissues and cells exhibit significantly elevated expression levels of ataxin 3 (ATXN3). Functional experiments demonstrated that ATXN3 promotes the invasion, migration, and tumor growth of GBM cells by activating EMT. Mechanistically, ATXN3 was identified as a bona fide deubiquitinase for ZEB1, a key EMT-inducing transcription factor, in GBM cells. ATXN3 interacts directly with ZEB1, cleaves ubiquitin moieties from conjugated substrates and maintains the stability of ZEB1. Ectopic expression of ZEB1 significantly mitigates the inhibitory effects of ATXN3 depletion on the invasion, migration, and tumor growth of GBM cells. Furthermore, ATXN3 exhibits a positive correlation with ZEB1 expression levels and serves as a predictor of poor prognosis in human GBM specimens. Collectively, our study elucidates a critical ATXN3-ZEB1 signaling axis in EMT and invasion, thereby providing a rationale for potential therapeutic interventions against GBM.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.