ArticleOncoTargets and therapy2020
UBE2O Promotes Progression and Epithelial-Mesenchymal Transition in Head and Neck Squamous Cell Carcinoma.
Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- The Oncogenic Role of Long Non-Coding RNABiology · 2026Review
- Ubiquitin-conjugating Enzymes in Cancer.International journal of biological sciences · 2026Review
- Post-translational modifications in the oral microenvironment: Stem cell regulation from periodontal regeneration to oral cancer therapy.World journal of stem cells · 2025Review
- Review
- The circular RNA hsa_circ_0045800 serves as a favorable biomarker in pathogenesis of sjögren's syndrome.Clinical rheumatology · 2024Article
- CircDCAF8 promotes the progression of hepatocellular carcinoma through miR-217/NAP1L1 Axis, and induces angiogenesis and regorafenib resistance via exosome-mediated transfer.Journal of translational medicine · 2024Article
- UBE2O reduces the effectiveness of interferon-α via degradation of IFIT3 in hepatocellular carcinoma.Cell death & disease · 2023Article
- High Level of Ubiquitin Conjugate Enzyme E2O Indicates Poor Prognosis of Patients with Hepatocellular Carcinoma.Current medical science · 2023Article
- Arborinine fromFood & nutrition research · 2022Article
- Ubiquitin-Conjugating Enzymes in Cancer.Cells · 2021Review
- The Molecular Basis of Ubiquitin-Conjugating Enzymes (E2s) as a Potential Target for Cancer Therapy.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundUBE2O, as a member of the ubiquitin-conjugating enzyme family, is abnormally expressed and exhibits abnormal functions in human malignancies. However, the function of UBE2O in head and neck squamous cell carcinoma (HNSCC) remains unknown. Therefore, our study aims to investigate the role of UBE2O in HNSCC progression and the underlying mechanisms.
methodsThe expression of UBE2O in HNSCC patients was investigated with data from the Cancer Genome Atlas (TCGA) and from a separate primary tumor cohort. The function of UBE2O in HNSCC cells was studied by cell viability assay, colony formation assay, wound healing assay, and cell migration and invasion chamber assay. The effect of UBE2O on tumor growth in vivo was determined in a subcutaneous xenograft model of HNSCC.
resultsTCGA data showed that UBE2O mRNA expression was dramatically increased in HNSCC tissues and that patients with high expression of UBE2O transcripts had a worse survival prognosis than patients with low expression of UBE2O transcripts. Gain-of-function and loss-of-function analyses revealed that oncogenic UBE2O enhanced the proliferation, migration and invasion of HNSCC cells in vitro. Further, mechanistic analysis revealed that UBE2O induced the epithelial-mesenchymal transition (EMT) phenotype and also potentiated TGF-β1-induced EMT, and thus leading to an enhanced capacity of migration and invasion in HNSCC. Finally, xenograft models showed that UBE2O knockout obviously inhibited the occurrence of EMT, angiogenesis and tumor growth in HNSCC in vivo.
conclusionOur study indicates that UBE2O acts as an oncogene to promote the malignant progression and EMT of HNSCC.
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