ArticleCell reports2013
An IKKα-nucleophosmin axis utilizes inflammatory signaling to promote genome integrity.
Article in Cell reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 26 citations in OpenAlex.
- Oral Fungal Infection Impacts Epithelial Innate Immunity to Promote Local and Distal Squamous Cell Carcinoma Progression.Cancer research · 2026Article
- The roles of IKKα in normal physiology and cancer.Cell communication and signaling : CCS · 2026Review
- Identified BIRC5 and HDAC1 as novel diagnostic biomarkers linked to centrosome-immune crosstalk for cutaneous squamous cell carcinoma via machine learning-based multi-omics analysis.Discover oncology · 2026Article
- Defective kinase activity of IKKα leads to combined immunodeficiency and disruption of immune tolerance in humans.Nature communications · 2024Article
- Review
- Sesamol Attenuates Renal Inflammation and Arrests Reactive-Oxygen-Species-Mediated IL-1β Secretion via the HO-1-Induced Inhibition of the IKKα/NFκB Pathway In Vivo and In Vitro.Antioxidants (Basel, Switzerland) · 2022Article
- A TNFR1-UBCH10 axis drives lung squamous cell carcinoma dedifferentiation and metastasis through a cell-autonomous signaling loop.Cell death & disease · 2022Article
- Centrosome Dynamics and Its Role in Inflammatory Response and Metastatic Process.Biomolecules · 2021Review
- EBP2, a novel NPM-ALK-interacting protein in the nucleolus, contributes to the proliferation of ALCL cells by regulating tumor suppressor p53.Molecular oncology · 2021Article
- PCNA and JNK1-Stat3 pathways respectively promotes and inhibits diabetes-associated centrosome amplification by targeting at the ROCK1/14-3-3σ complex in human colon cancer HCT116 cells.Journal of cellular physiology · 2019Article
- IKKα inactivation promotes Kras-initiated lung adenocarcinoma development through disrupting major redox regulatory pathways.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Baicalin hydrate inhibits cancer progression in nasopharyngeal carcinoma by affecting genome instability and splicing.Oncotarget · 2018Article
- Autoreactive T Cells and Chronic Fungal Infection Drive Esophageal Carcinogenesis.Cell host & microbe · 2017Article
- LGR5 expression is controled by IKKα in basal cell carcinoma through activating STAT3 signaling pathway.Oncotarget · 2016Article
- A feedforward loop of NLRC5 (de)ubiquitination keeps IKK-NF-κB in check.The Journal of cell biology · 2015Article
- Genomic instability in human cancer: Molecular insights and opportunities for therapeutic attack and prevention through diet and nutrition.Seminars in cancer biology · 2015Review
- Cytoplasmic nucleophosmin has elevated T199 phosphorylation upon which G2/M phase progression is dependent.Scientific reports · 2015Article
- Identification of novel DNA-damage tolerance genes reveals regulation of translesion DNA synthesis by nucleophosmin.Nature communications · 2014Article
Corrections and comments
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Authors and funding
15 authors at 7 institutions in 1 country.
Funding
Abstract
The inflammatory microenvironment promotes skin tumorigenesis. However, the mechanisms by which cells protect themselves from inflammatory signals are unknown. Downregulation of IKKα promotes skin tumor progression from papillomas to squamous cell carcinomas, which is frequently accompanied by genomic instability, including aneuploid chromosomes and extra centrosomes. In this study, we found that IKKα promoted oligomerization of nucleophosmin (NPM), a negative centrosome duplication regulator, which further enhanced NPM and centrosome association, inhibited centrosome amplification, and maintained genome integrity. Levels of NPM hexamers and IKKα were conversely associated with skin tumor progression. Importantly, proinflammatory cytokine-induced IKKα activation promoted the formation of NPM oligomers and reduced centrosome numbers in mouse and human cells, whereas kinase-dead IKKα blocked this connection. Therefore, our findings suggest a mechanism in which an IKKα-NPM axis may use inflammatory signals to suppress centrosome amplification, promote genomic integrity, and prevent tumor progression.
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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.