ArticleMolecular biology reports2025
UBE3C promotes pancreatic ductal adenocarcinoma progression by catalysing p53 ubiquitination.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Ubiquitination and NOncology letters · 2026Review
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Authors and funding
6 authors.
Funding
Abstract
backgroundPancreatic ductal adenocarcinoma (PDAC) is among the deadliest malignancies worldwide. Ubiquitination is a biological process that regulates the degradation of proteins. Previous studies have indicated that ubiquitin ligase E3C (UBE3C) has procarcinogenic properties in various tumours. Nevertheless, the detailed role of UBE3C in PDAC is still unknown. METHODS AND
resultsBioinformatics analyses of UBE3C were performed, and we found that UBE3C expression was increased in PDAC cells and indicates a poorer clinical prognosis. Moreover, a significant positive correlation existed between UBE3C expression and the number of CD4
conclusionsOur results clarify the importance of UBE3C in PDAC and indicate that the UBE3C-p53 axis may be a novel therapeutic target for PDAC. CLINICAL TRIAL NUMBER: Not applicable.
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