ArticleCarcinogenesis2007
Nucleophosmin suppresses oncogene-induced apoptosis and senescence and enhances oncogenic cooperation in cells with genomic instability.
Article in Carcinogenesis, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 29 citations in OpenAlex.
- Peptide aptamer sP10 targeting NPM1 attenuates liver fibrosis and hepatocellular carcinoma.Journal of translational medicine · 2026Article
- Nucleophosmin Interacts with PIN2/TERF1-interacting Telomerase Inhibitor 1 (PinX1) and Attenuates the PinX1 Inhibition on Telomerase Activity.Scientific reports · 2017Article
- The endocrine disruptor cadmium alters human osteoblast-like Saos-2 cells homeostasis in vitro by alteration of Wnt/β-catenin pathway and activation of caspases.Journal of endocrinological investigation · 2015Article
- Interactions of the natural product (+)-avrainvillamide with nucleophosmin and exportin-1 Mediate the cellular localization of nucleophosmin and its AML-associated mutants.ACS chemical biology · 2015Article
- Tumour suppressor HLJ1: A potential diagnostic, preventive and therapeutic target in non-small cell lung cancer.World journal of clinical oncology · 2014Review
- Nucleophosmin is essential for c-Myc nucleolar localization and c-Myc-mediated rDNA transcription.Oncogene · 2013Article
- An analysis of substitution, deletion and insertion mutations in cancer genes.Nucleic acids research · 2012Article
- Nucleophosmin and its complex network: a possible therapeutic target in hematological diseases.Oncogene · 2011Review
- Nucleolar stress is an early response to myocardial damage involving nucleolar proteins nucleostemin and nucleophosmin.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- MYC as a regulator of ribosome biogenesis and protein synthesis.Nature reviews. Cancer · 2010Review
- NPM phosphorylation stimulates Cdk1, overrides G2/M checkpoint and increases leukemic blasts in mice.Carcinogenesis · 2010Article
- The Myc-nucleophosmin-ARF network: a complex web unveiled.Cell cycle (Georgetown, Tex.) · 2009Review
- Absence of caspase-3 protects pancreatic {beta}-cells from c-Myc-induced apoptosis without leading to tumor formation.The Journal of biological chemistry · 2009Article
- Antioxidant intervention of smoking-induced lung tumor in mice by vitamin E and quercetin.BMC cancer · 2008Article
- Nucleophosmin interacts directly with c-Myc and controls c-Myc-induced hyperproliferation and transformation.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Inflammation and endothelial dysfunction during aging: role of NF-kappaB.Journal of applied physiology (Bethesda, Md. : 1985) · 2008Review
- Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Cells from patients with genomic instability syndromes have high predisposition to cancer. However, little is known about whether these mutant cells have high susceptibility to oncogenic transformation. We have tested the hypothesis that a defect in maintaining genome integrity is necessary but not sufficient alone for oncogenic transformation and needs to collaborate with other signals in order to produce full oncogenic transformation. Using genetically matched primary cells deficient for the Fanconi complementation group C gene (Fancc) and the ataxia telangiectasia mutated gene (Atm), we found that certain forms of oncogenic activation and cooperation require a combination of genomic instability with increased expression of nucleophosmin (NPM) to prevent oncogenic stress-induced apoptosis or senescence. Intriguingly, co-expression of c-Myc and NPM leads to a synergistic increase in the proliferation rate in Fancc-/- or Atm-/- cells. Analysis of p53 stabilization and activation by c-Myc demonstrates that over-expression of NPM significantly reduces the accumulation of the activated p53 but not the stability of p53. Moreover, NPM is shown to enhance transforming activity of co-expressed Myc and Ras in wild-type and, to a greater degree, in Fancc-/- or Atm-/- cells, suggesting a role in oncogenic cooperation. Finally, a partial knockdown of NPM is sufficient to cause massive apoptosis in Fancc-/- or Atm-/- cells co-expressing c-Myc and Ras while sparing untransformed cells. Our study demonstrates a novel mechanism of NPM tumorigenesis by establishing NPM as a crucial inhibitor of oncogene-induced apoptosis and senescence.
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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.