ArticleCell death & disease2023
UBE2O reduces the effectiveness of interferon-α via degradation of IFIT3 in hepatocellular carcinoma.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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
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.
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Who cites it
8 citing papers in PubMed, 20 citations in OpenAlex.
- Integrative multi-omics analysis reveals IFIT3⁺ macrophage-associated ISG20 as a prognostic biomarker and elucidates underlying tumor-suppressive mechanisms in ovarian cancer.Journal of ovarian research · 2026Article
- Melatonin attenuates inflammatory bone loss by alleviating mitophagy and lactate production.Apoptosis : an international journal on programmed cell death · 2025Article
- Mycobacterium tuberculosis hijacks the UBE2O pathway to regulate host iron homeostasis.The Journal of clinical investigation · 2025Article
- Review
- IFIT3: a crucial mediator in innate immunity and tumor progression with therapeutic implications.Frontiers in immunology · 2025Review
- Advances in immunotherapy for hepatitis B virus associated hepatocellular carcinoma patients.World journal of hepatology · 2024Review
- The Ubiquitin-Conjugating Enzyme E2 O (UBE2O) and Its Therapeutic Potential in Human Leukemias and Solid Tumors.Cancers · 2024Review
- 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
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interferon (IFN) exerts its effects through interferon-stimulated genes (ISGs), but its efficacy is limited by interferon resistance, which can be caused by the ubiquitination of key proteins. UBE2O was initially identified as a promising therapeutic target based on data from the TCGA and iUUCD 2.0 databases. Through the inhibition of UBE2O, interferon α/β signaling and overall interferon signaling were activated. Integrating data from proteomic, mass spectrometry, and survival analyses led to the identification of IFIT3, a mediator of interferon signaling, as a ubiquitination substrate of UBE2O. The results of in vitro and in vivo experiments demonstrated that the knockdown of UBE2O can enhance the efficacy of interferon-α by upregulating IFIT3 expression. K236 was identified as a ubiquitination site in IFIT3, and the results of rescue experiments confirmed that the effect of UBE2O on interferon-α sensitivity is dependent on IFIT3 activity. ATO treatment inhibited UBE2O and increased IFIT3 expression, thereby increasing the effectiveness of interferon-α. In conclusion, these findings suggest that UBE2O worsens the therapeutic effect of interferon-α by targeting IFIT3 for ubiquitination and degradation.
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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.