ArticleMolecular cancer therapeutics2012
Evidence for the ubiquitin protease UBP43 as an antineoplastic target.
Article in Molecular cancer therapeutics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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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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
28 citing papers in PubMed, 45 citations in OpenAlex.
- Article
- The ISGylation tapestry in cancer: weaving phenotypic plasticity through multidimensional regulatory looms.Cellular & molecular biology letters · 2025Review
- Review
- Chemical tools to define and manipulate interferon-inducible Ubl protease USP18.Nature communications · 2025Article
- Article
- Chemical tools to define and manipulate interferon-inducible Ubl protease USP18.bioRxiv : the preprint server for biology · 2024Article
- ISG15 mediates the function of extracellular vesicles in promoting ovarian cancer progression and metastasis.Journal of extracellular biology · 2024Article
- ISGylation-independent protection of cell growth by USP18 following interferon stimulation.The Biochemical journal · 2023Article
- USP18 is an essential regulator of muscle cell differentiation and maturation.Cell death & disease · 2023Article
- Loss of ubiquitin-specific peptidase 18 destabilizes 14-3-3ζ protein and represses lung cancer metastasis.Cancer biology & therapy · 2022Article
- ISG15 and ISGylation in Human Diseases.Cells · 2022Review
- High expression of USP18 is associated with the growth of colorectal carcinoma.Histology and histopathology · 2021Article
- The Ubiquitin-Specific Peptidase USP18 Promotes Lipolysis, Fatty Acid Oxidation, and Lung Cancer Growth.Molecular cancer research : MCR · 2021Article
- Emerging Roles of USP18: From Biology to Pathophysiology.International journal of molecular sciences · 2020Review
- Exploring DNA Methylation Profiles Altered in Cryptogenic Hepatocellular Carcinomas by High-Throughput Targeted DNA Methylation Sequencing: A Preliminary Study for Cryptogenic Hepatocellular Carcinoma.OncoTargets and therapy · 2020Article
- Upregulation of Enzymes involved in ISGylation and Ubiquitination in patients with hepatocellular carcinoma.International journal of medical sciences · 2020Article
- Evidence for the ISG15-Specific Deubiquitinase USP18 as an Antineoplastic Target.Cancer research · 2018Review
- Deubiquitinase USP18 Loss Mislocalizes and Destabilizes KRAS in Lung Cancer.Molecular cancer research : MCR · 2017Article
- The ISG15-specific protease USP18 regulates stability of PTEN.Oncotarget · 2017Article
- Multiple functions of USP18.Cell death & disease · 2016Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
New pharmacologic targets are needed for lung cancer. One candidate pathway to target is composed of the E1-like ubiquitin-activating enzyme (UBE1L) that associates with interferon-stimulated gene 15 (ISG15), which complexes with and destabilizes cyclin D1. Ubiquitin protease 43 (UBP43/USP18) removes ISG15 from conjugated proteins. This study reports that gain of UBP43 stabilized cyclin D1, but not other D-type cyclins or cyclin E. This depended on UBP43 enzymatic activity; an enzymatically inactive UBP43 did not affect cyclin D1 stability. As expected, small interfering RNAs that reduced UBP43 expression also decreased cyclin D1 levels and increased apoptosis in a panel of lung cancer cell lines. Forced cyclin D1 expression rescued UBP43 apoptotic effects, which highlighted the importance of cyclin D1 in conferring this. Short hairpin RNA-mediated reduction of UBP43 significantly increased apoptosis and reduced murine lung cancer growth in vitro and in vivo after transplantation of these cells into syngeneic mice. These cells also exhibited increased response to all-trans-retinoic acid, interferon, or cisplatin treatments. Notably, gain of UBP43 expression antagonized these effects. Normal-malignant human lung tissue arrays were examined independently for UBP43, cyclin D1, and cyclin E immunohistochemical expression. UBP43 was significantly (P < 0.01) increased in the malignant versus normal lung. A direct relationship was found between UBP43 and cyclin D1 (but not cyclin E) expression. Differential UBP43 expression was independently detected in a normal-malignant tissue array with diverse human cancers. Taken together, these findings uncovered UBP43 as a previously unrecognized antineoplastic target.
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Registered trials
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