ArticleOncotarget2016
Interferon-stimulated gene 15 induces cancer cell death by suppressing the NF-κB signaling pathway.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Understanding protein ISGylation, a multifaceted posttranslational modification.Cell chemical biology · 2026Review
- The ISGylation tapestry in cancer: weaving phenotypic plasticity through multidimensional regulatory looms.Cellular & molecular biology letters · 2025Review
- Review
- Analysis of head and neck cancer scRNA-seq data identified PRDM6 promotes tumor progression by modulating immune gene expression.Frontiers in immunology · 2025Article
- Molecular Interplay of ISG15/ISGylation in Neuropathologies.CNS & neurological disorders drug targets · 2025Review
- Literature review: nuclear factor kappa B (NF-κB) regulation in human cancers mediated by ubiquitin-specific proteases (USPs).Annals of translational medicine · 2024Review
- Single-cell transcriptomes and chromatin accessibility of endothelial cells unravel transcription factors associated with dysregulated angiogenesis in systemic sclerosis.Annals of the rheumatic diseases · 2024Article
- ISGylation of NF-κBp65 by SCFArteriosclerosis, thrombosis, and vascular biology · 2023Article
- Protein ISGylation: a posttranslational modification with implications for malignant neoplasms.Exploration of targeted anti-tumor therapy · 2023Review
- The diverse repertoire of ISG15: more intricate than initially thought.Experimental & molecular medicine · 2022Review
- ISG15 deficiency features a complex cellular phenotype that responds to treatment with itaconate and derivatives.Clinical and translational medicine · 2022Article
- ISGylation Inhibits an LPS-Induced Inflammatory Response via the TLR4/NF-κB Signaling Pathway in Goat Endometrial Epithelial Cells.Animals : an open access journal from MDPI · 2021Article
- Increased expression of IFI16 predicts adverse prognosis in multiple myeloma.The pharmacogenomics journal · 2021Article
- Dual EZH2 and G9a inhibition suppresses multiple myeloma cell proliferation by regulating the interferon signal and IRF4-MYC axis.Cell death discovery · 2021Article
- Emerging Roles of USP18: From Biology to Pathophysiology.International journal of molecular sciences · 2020Review
- Loss of TRIM29 suppresses cancer stem cell-like characteristics of PDACs via accelerating ISG15 degradation.Oncogene · 2020Article
- Interferons α and β in cancer: therapeutic opportunities from new insights.Nature reviews. Drug discovery · 2019Review
- Evidence for the ISG15-Specific Deubiquitinase USP18 as an Antineoplastic Target.Cancer research · 2018Review
- Covalent ISG15 conjugation to CHIP promotes its ubiquitin E3 ligase activity and inhibits lung cancer cell growth in response to type I interferon.Cell death & disease · 2018Article
- Cell type-dependent regulation of free ISG15 levels and ISGylation.Journal of cell communication and signaling · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interferon-stimulated gene 15 (ISG15) is an important cytokine that has been reported in carcinogenesis. However, we found that ISG15 and de-ISGylase USP18 were induced by several anti-cancer agents, which was confirmed by both RT-PCR and immunoblotting assays. Further studies demonstrated that ectopic ISG15 and USP18 inhibited proliferation of myeloma, leukemia and cervical cancer cells. More importantly, ISG15 and USP18 induced cancer cell apoptosis. This finding was confirmed in a cervical xenograft model in which cervical cancer growth was suppressed by lentiviral ISG15. In the mechanistic study, ISG15 was found to disrupt the NF-κB signaling pathway by downregulating the expression of IKKβ and p65, phosphorylation of p65 and IκBα. Consistent with this finding, ISG15 suppressed the expression of NF-κB recognition element-driving luciferase and decreased the transcription of XIAP and Mcl-1, two typical genes regulated by NF-κB. Therefore, the present study demonstrated that ISG15 induces cancer cell apoptosis by disrupting the NF-κB signaling pathway. This study highlighted a novel role of ISG15 in tumor suppression.
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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.