ArticleBMC cancer2026
UBA1 drives cell cycle to promote malignancy and serves as a therapeutic target in Ewing Sarcoma.
Article in BMC cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEwing sarcoma (ES) is an aggressive malignancy with high metastatic potential and poor prognosis, necessitating novel biomarkers and therapeutic targets. This study investigates the role of the ubiquitin-activating enzyme E1 (UBA1) in ES pathogenesis and its clinical relevance.
methodsBioinformatic analysis of GEO datasets was performed. UBA1 expression was validated in clinical samples and ES cell lines (A673, RDES) via Western blot and qPCR. To investigate the functional role and therapeutic potential of UBA1 in ES, we performed siRNA-mediated knockdown followed by a series of in vitro functional assays, including assessments of proliferation, colony formation, migration, invasion, cell cycle distribution, and EdU incorporation. Mechanistic studies were subsequently conducted through the WB experiment. In vivo experiments were carried out using a xenograft mouse model to evaluate the effect of UBA1 depletion on tumor growth. Additionally, the UBA1-specific inhibitor TAK-243 was used to assess the therapeutic potential of targeting UBA1.
resultsUBA1 expression was significantly elevated in ES tissues, and high UBA1 levels correlated with poor prognosis. Knockdown of UBA1 suppressed malignant phenotypes, including proliferation, colony formation, migration, and invasion, while inducing cell cycle arrest and inhibiting DNA synthesis. Mechanistically, UBA1 depletion led to dysregulation of the G2/M checkpoint pathway, consistent with Gene Set Enrichment Analysis (GSEA) predictions. In vivo experiments confirmed the oncogenic role of UBA1, and treatment with the UBA1 inhibitor TAK-243 recapitulated the effects observed upon UBA1 knockdown.
conclusionTargeting UBA1 disrupts cell cycle progression and inhibits proliferation in ES, underscoring its therapeutic potential.
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.