ArticleOncology letters2025
UBE2T promotes epithelial-mesenchymal transition and motility in oral cancer cells via induction of IL-6 expression.
Article in Oncology letters, 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.
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Who cites it
1 citing paper in PubMed.
- Post-translational modifications in the oral microenvironment: Stem cell regulation from periodontal regeneration to oral cancer therapy.World journal of stem cells · 2025Review
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oral squamous cell carcinoma (OSCC) is a prevalent aggressive malignancy with a high mortality rate. However, the mechanisms underlying the progression of OSCC remain to be elucidated. In the present study, bioinformatics analysis identified ubiquitin-conjugating enzyme E2 T (UBE2T) as a poor prognostic factor in head and neck cancer, showing the strongest association with cancer stage progression. Functional studies revealed that UBE2T can enhance motility and induce epithelial-mesenchymal transition (EMT) in OSCC cells. RNA sequencing and subsequent analyses demonstrated that UBE2T upregulated the expression levels of various motility- and EMT-related factors, including ankyrin repeat domain 1, endothelin-1, interleukin-6 (IL-6), matrix metalloproteinase-9 and plasminogen activator, urokinase. Gene set enrichment analysis indicated that UBE2T activates the IL-6/Janus protein tyrosine kinase (JAK)/signal transducer and activator of transcription 3 signaling pathway. Moreover, treatment of OSCC cells with IL-6 or a JAK inhibitor resulted in the induction of EMT and mesenchymal-epithelial transition, respectively, accompanied by enhanced and suppressed cancer cell motility. These results indicated that IL-6, which is upregulated by UBE2T, may be crucial for maintaining mesenchymal traits and motility in OSCC cells. Collectively, these findings suggested that the UBE2T/IL-6/JAK axis may serve as a potential therapeutic target for OSCC.
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