ArticleNaunyn-Schmiedeberg's archives of pharmacology2025
Deubiquitinase USP28 promotes the malignant progression and radio-resistance of hepatocellular carcinoma by stabilizing WDHD1.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Post-translational modification networks in tumor radiosensitivity: mechanistic insights and therapeutic opportunities.Journal of translational medicine · 2026Review
- Targeting the deubiquitinase USP28 in cancer: navigating context-dependent mechanisms and therapeutic resistance.Frontiers in immunology · 2026Review
- Activation of WDHD1 by DNA demethylases promotes MINPP1 transcription and glycolysis in lung adenocarcinoma progression.Respiratory research · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Radio-resistance is a principal culprit in radiation therapy for hepatocellular carcinoma (HCC). Insights on the regulation genes of radio-resistance and underlying mechanisms in HCC are awaiting profound investigation. This study is designed to explore the role and mechanism of WD repeat and HMG-box DNA binding protein 1 (WDHD1) in HCC progression. WDHD1 mRNA level was detected using real-time quantitative polymerase chain reaction (RT-qPCR). WDHD1, ubiquitin-specific protease 28 (USP28), E-cadherin, N-cadherin, and vimentin protein levels were determined by Western blot. Cell viability, cell cycle progression, migration, invasion, and apoptosis were assessed using the cell counting kit-8 (CCK-8) assay, flow cytometry, wound healing assay, and Transwell assay. The radio-sensitivity of HCC cells was analyzed using a colony formation assay. After UbiBrowser database analysis, the interaction between USP28 and WDHD1 was verified using GST pull-down and Co-immunoprecipitation (CoIP) assay. Xenograft assay was used to test the effect of USP28 on radio-sensitivity in vivo. WDHD1 and USP28 were highly expressed in HCC patients and cell lines. Moreover, WDHD1 knockdown could repress HCC cell proliferation, migration, invasion, epithelial to mesenchymal transition (EMT), and enhance the radiosensitivity. Mechanistically, USP28 mediated the deubiquitination and stabilization of WDHD1 through its direct interaction. USP28 silencing increased the radiosensitivity of HCC in vivo. USP28 contributed to HCC development and radio-resistance through deubiquitinating WDHD1, providing a promising therapeutic target for HCC treatment.
Indexed as
Identifiers
39928151What 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.