ArticleCell biochemistry and biophysics2025
USP5 Stabilizes IKBKG Through Deubiquitination to Suppress Ferroptosis and Promote Growth in Non-small Cell Lung Cancer.
Article in Cell biochemistry and biophysics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- USP5 in cancer: a therapeutic window into metabolism and drug resistance.Journal of translational medicine · 2026Review
- USP5 promotes glycolysis in cervical cancer by stabilizing FOXM1.American journal of cancer research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ferroptosis, a distinctive modality of cell mortality, has emerged as a critical regulator in non-small cell lung cancer (NSCLC). The deubiquitinating enzyme USP5 has established an oncogenic role in NSCLC. However, its biological relevance in NSCLC cell ferroptosis is currently unexplored. Expression analysis was performed by quantitative PCR (qPCR), immunohistochemistry (IHC) and immunoblotting. Animal xenograft studies were used to detect USP5's role in tumor growth. Cell proliferation, colony formation and apoptotic ratio were assessed by CCK-8, colony formation and flow cytometry assays, respectively. Cell ferroptosis was evaluated by gauging ROS, MDA, GSH, SOD, and Fe
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Registered trials
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