ReviewCell cycle (Georgetown, Tex.)2009
The Myc-nucleophosmin-ARF network: a complex web unveiled.
Review in Cell cycle (Georgetown, Tex.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 53 citations in OpenAlex.
- In-depth inference of transcriptional regulatory networks reveals NPM1 as a therapeutic ribosomal regulator in MYC-amplified medulloblastoma.NPJ precision oncology · 2025Article
- A "grappling hook" interaction connects self-assembly and chaperone activity of Nucleophosmin 1.PNAS nexus · 2023Article
- Carcinogen-induced super-enhancer RNA promotes nasopharyngeal carcinoma metastasis through NPM1/c-Myc/NDRG1 axis.American journal of cancer research · 2023Article
- Regulation of Nucleolar Activity by MYC.Cells · 2022Review
- tp53-dependent and independent signaling underlies the pathogenesis and possible prevention of Acrofacial Dysostosis-Cincinnati type.Human molecular genetics · 2018Article
- Analysis of the oligomeric states of nucleophosmin using size exclusion chromatography.Scientific reports · 2018Article
- Nucleolar stress: is there a reverse version?Journal of Cancer · 2018Article
- Cancer upregulated gene 2 induces epithelial-mesenchymal transition of human lung cancer cells via TGF-β signaling.Oncotarget · 2017Article
- Expression, function, and targeting of the nuclear exporter chromosome region maintenance 1 (CRM1) protein.Pharmacology & therapeutics · 2015Review
- Down-regulated expression of NPM1 in IMS-M2 cell line by (-)-epigallocatechin-3-gallate.Asian Pacific journal of tropical biomedicine · 2014Article
- MYC cofactors: molecular switches controlling diverse biological outcomes.Cold Spring Harbor perspectives in medicine · 2014Review
- Structural polymorphism in the N-terminal oligomerization domain of NPM1.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Preferential autoimmune response in prostate cancer to cyclin B1 in a panel of tumor-associated antigens.Journal of immunology research · 2014Article
- Identification of O-GlcNAc modification targets in mouse retinal pericytes: implication of p53 in pathogenesis of diabetic retinopathy.PloS one · 2014Article
- Article
- Nucleophosmin is essential for c-Myc nucleolar localization and c-Myc-mediated rDNA transcription.Oncogene · 2013Article
- Domain-specific c-Myc ubiquitylation controls c-Myc transcriptional and apoptotic activity.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Article
- Regulation of subcellular distribution and oncogenic potential of nucleophosmin by plakoglobin.Oncogenesis · 2012Article
- Knockdown of nucleophosmin induces S-phase arrest in HepG2 cells.Chinese journal of cancer · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The multifunctional nucleolar proteins, nucleophosmin (NPM) and the tumor suppressor ARF, have been assigned numerous roles in diverse cellular processes impacting cellular proliferation, tumorigenesis and apoptosis. In addition, both proteins have been linked to the oncogenic function of c-Myc, a transcription factor that drives the majority of human cancers. Both proteins are induced by oncogenic c-Myc, but have opposing outcomes. Whereas loss of ARF accelerates c-Myc-induced tumorigenesis, NPM overexpression enhances c-Myc transformation. Accordingly, ARF expression is lost in many tumors, while NPM expression is elevated. Previously, we demonstrated that ARF interacts directly with c-Myc, leading to inhibition of its transforming activity while enhancing its apoptotic activity, independently of p53. We have recently shown that NPM also binds directly to c-Myc, but with opposite effects compared to ARF. NPM dramatically enhances the oncogenic activity of c-Myc, independently of ARF and p53. In tumor cells, the ARF-p53 pathway is often inactivated while NPM is elevated. However, when NPM and ARF are both expressed with oncogenic c-Myc the outcome of the interactions becomes more complex, since NPM and ARF also interact directly and NPM controls ARF localization. In this report we demonstrate that in the presence of ARF, NPM overexpression dramatically inhibits c-Myc-induced p53-independent apoptosis, while enhancing proliferation and transformation. We find that NPM sequesters ARF in nucleoli, blocking the relocalization of ARF to the nucleoplasm caused by activation of c-Myc. Therefore, the fate of a cell to undergo apoptosis or become transformed is dependent on this complex interacting network of oncogenic and tumor suppressor proteins.
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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.