Evidence map›Paper›PMID 20190806›Full record

ArticleOncogene2010

Bmi1 is a MYCN target gene that regulates tumorigenesis through repression of KIF1Bbeta and TSLC1 in neuroblastoma.

H Ochiai, H Takenobu, A Nakagawa, Y Yamaguchi, M Kimura, M Ohira, Y Okimoto, Y Fujimura, H Koseki, Y Kohno and 2 more

Abstract read
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In one paragraph

Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

46 citing papers in PubMed, 83 citations in OpenAlex.

  1. Targeting MYC-Driven Cancers: From Oncogenic Addiction to Therapeutic Vulnerability.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026
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  4. Molecular regulation and therapeutic targeting ofFrontiers in cell and developmental biology · 2025
    Review
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  7. An immature, dedifferentiated, and lineage-deconstrained cone precursor origin of N-Myc-initiated retinoblastoma.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Cancer stem cells in neuroblastoma therapy resistance.Cancer drug resistance (Alhambra, Calif.) · 2019
    Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 5 institutions in 1 country.

H OchiaiDivision of Biochemistry and Molecular Carcinogenesis, Chiba Cancer Center Research Institute, Chiba, Japan.
H Takenobu
A Nakagawa
Y Yamaguchi
M Kimura
M Ohira
Y Okimoto
Y Fujimura
H Koseki
Y Kohno
A Nakagawara
T Kamijo
Chiba Cancer Center · JPRIKEN Center for Integrative Medical Sciences · JPChiba Hospital · JPChiba University · JPNational Center For Child Health and Development · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent advances in neuroblastoma (NB) research addressed that epigenetic alterations such as hypermethylation of promoter sequences, with consequent silencing of tumor-suppressor genes, can have significant roles in the tumorigenesis of NB. However, the exact role of epigenetic alterations, except for DNA hypermethylation, remains to be elucidated in NB research. In this paper, we clarified the direct binding of MYCN to Bmi1 promoter and upregulation of Bmi1 transcription by MYCN. Mutation introduction into an MYCN binding site in the Bmi1 promoter suggests that MYCN has more important roles in the transcription of Bmi1 than E2F-related Bmi1 regulation. A correlation between MYCN and polycomb protein Bmi1 expression was observed in primary NB tumors. Expression of Bmi1 resulted in the acceleration of proliferation and colony formation in NB cells. Bmi1-related inhibition of NB cell differentiation was confirmed by neurite extension assay and analysis of differentiation marker molecules. Intriguingly, the above-mentioned Bmi1-related regulation of the NB cell phenotype seems not to be mediated only by p14ARF/p16INK4a in NB cells. Expression profiling analysis using a tumor-specific cDNA microarray addressed the Bmi1-dependent repression of KIF1Bbeta and TSLC1, which have important roles in predicting the prognosis of NB. Chromatin immunoprecipitation assay showed that KIF1Bbeta and TSLC1 are direct targets of Bmi1 in NB cells. These findings suggest that MYCN induces Bmi1 expression, resulting in the repression of tumor suppressors through Polycomb group gene-mediated epigenetic chromosome modification. NB cell proliferation and differentiation seem to be partially dependent on the MYCN/Bmi1/tumor-suppressor pathways.

Indexed as

Cell Adhesion Molecule-1Cell Adhesion MoleculesCell DifferentiationCell Line, TumorCell ProliferationGenes, Tumor SuppressorHumansImmunoglobulinsKinesinsMembrane ProteinsNeuroblastomaN-Myc Proto-Oncogene ProteinNuclear ProteinsOncogene ProteinsPolycomb Repressive Complex 1Promoter Regions, GeneticBMI1 protein, humanCADM1 protein, humanCell Adhesion Molecule-1Cell Adhesion MoleculesImmunoglobulinsKIF1B protein, humanKinesinsMembrane ProteinsMYCN protein, humanN-Myc Proto-Oncogene ProteinNuclear ProteinsOncogene ProteinsPolycomb Repressive Complex 1Proto-Oncogene ProteinsRepressor ProteinsTumor Suppressor Proteins

Identifiers

PMID20190806
OpenAlexW2022452105

What OpenQuestion holds

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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.