Evidence map›Paper›PMID 24727676›Full record

ArticleLeukemia2014

Notch and NF-kB signaling pathways regulate miR-223/FBXW7 axis in T-cell acute lymphoblastic leukemia.

V Kumar, R Palermo, C Talora, A F Campese, S Checquolo, D Bellavia, L Tottone, G Testa, E Miele, S Indraccolo and 5 more

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed
6.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

103 citing papers in PubMed, 186 citations in OpenAlex.

  1. Review
  2. Article
  3. Acta pharmaceutica Sinica. B · 2025
    Article
  4. Review
  5. Notch Inhibitors and BH3 Mimetics in T-Cell Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2024
    Review
  6. Molecular insights and clinical implications for the tumor suppressor role of SCFBiochimica et biophysica acta. Reviews on cancer · 2024
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Different miRNAs Related toInternational journal of molecular sciences · 2023
    Article
  13. Article
  14. Notch Partners in the Long Journey of T-ALL Pathogenesis.International journal of molecular sciences · 2023
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. miRNAs in Lymphocytic Leukaemias-The miRror of Drug Resistance.International journal of molecular sciences · 2022
    Review

43 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 4 institutions in 1 country.

V KumarLaboratory of Molecular Pathology, Department of Molecular Medicine, Sapienza University, Rome, Italy.
R PalermoCenter for Life Nano Science@Sapienza, Istituto Italiano di Tecnologia, Rome, Italy.
C TaloraLaboratory of Molecular Pathology, Department of Molecular Medicine, Sapienza University, Rome, Italy.
A F CampeseLaboratory of Molecular Pathology, Department of Molecular Medicine, Sapienza University, Rome, Italy.
S ChecquoloDepartment of Medico-Surgical Sciences and Biotechnology, Sapienza University, Latina, Italy.
D BellaviaLaboratory of Molecular Pathology, Department of Molecular Medicine, Sapienza University, Rome, Italy.
L TottoneLaboratory of Molecular Pathology, Department of Molecular Medicine, Sapienza University, Rome, Italy.
G TestaLaboratory of Molecular Pathology, Department of Molecular Medicine, Sapienza University, Rome, Italy.
E MieleCenter for Life Nano Science@Sapienza, Istituto Italiano di Tecnologia, Rome, Italy.ORCID 0000000247471032
S IndraccoloIstituto Oncologico Veneto-IRCCS-Padova, Padua, Italy.
A Amadori1] Istituto Oncologico Veneto-IRCCS-Padova, Padua, Italy [2] Department of Surgery, Oncology and Gastroenterology, University of Padua, Padua, Italy.
E FerrettiDepartment of Experimental Medicine, Sapienza University, Rome, Italy.
A Gulino1] Laboratory of Molecular Pathology, Department of Molecular Medicine, Sapienza University, Rome, Italy [2] Center for Life Nano Science@Sapienza, Istituto Italiano di Tecnologia, Rome, Italy [3] Neuromed Institute, Pozzilli, Italy.
A VaccaDepartment of Experimental Medicine, Sapienza University, Rome, Italy.
I Screpanti1] Laboratory of Molecular Pathology, Department of Molecular Medicine, Sapienza University, Rome, Italy [2] Center for Life Nano Science@Sapienza, Istituto Italiano di Tecnologia, Rome, Italy [3] Institute Pasteur-Foundation Cenci Bolognetti, Sapienza University, Rome, Italy.
Sapienza University of Rome · ITItalian Institute of Technology · ITIstituto Oncologico Veneto · ITUniversity of Padua · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Notch signaling deregulation is linked to the onset of several tumors including T-cell acute lymphoblastic leukemia (T-ALL). Deregulated microRNA (miRNA) expression is also associated with several cancers, including leukemias. However, the transcriptional regulators of miRNAs, as well as the relationships between Notch signaling and miRNA deregulation, are poorly understood. To identify miRNAs regulated by Notch pathway, we performed microarray-based miRNA profiling of several Notch-expressing T-ALL models. Among seven miRNAs, consistently regulated by overexpressing or silencing Notch3, we focused our attention on miR-223, whose putative promoter analysis revealed a conserved RBPjk binding site, which was nested to an NF-kB consensus. Luciferase and chromatin immunoprecipitation assays on the promoter region of miR-223 show that both Notch and NF-kB are novel coregulatory signals of miR-223 expression, being able to activate cooperatively the transcriptional activity of miR-223 promoter. Notably, the Notch-mediated activation of miR-223 represses the tumor suppressor FBXW7 in T-ALL cell lines. Moreover, we observed the inverse correlation of miR-223 and FBXW7 expression in a panel of T-ALL patient-derived xenografts. Finally, we show that miR-223 inhibition prevents T-ALL resistance to γ-secretase inhibitor (GSI) treatment, suggesting that miR-223 could be involved in GSI sensitivity and its inhibition may be exploited in target therapy protocols.

Indexed as

Gene Expression Regulation, LeukemicSignal TransductionAmyloid Precursor Protein SecretasesAnimalsCell Cycle ProteinsCell Line, TumorCell ProliferationCluster AnalysisDipeptidesDisease Models, AnimalDrug Resistance, NeoplasmF-Box ProteinsF-Box-WD Repeat-Containing Protein 7Gene Expression ProfilingGene SilencingHumansAmyloid Precursor Protein SecretasesCell Cycle ProteinsDipeptidesF-Box ProteinsF-Box-WD Repeat-Containing Protein 7FBXW7 protein, humanMicroRNAsMIR223, humanNF-kappa BN-(N-(3,5-difluorophenacetyl)alanyl)phenylglycine tert-butyl esterReceptors, NotchUbiquitin-Protein Ligases

Identifiers

PMID24727676
OpenAlexW1985405118

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Registered trials

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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.