Evidence map›Paper›PMID 17452456›Full record

ArticleMolecular and cellular biology2007

Contribution of polycomb homologues Bmi-1 and Mel-18 to medulloblastoma pathogenesis.

Dmitri Wiederschain, Lin Chen, Brett Johnson, Kimberly Bettano, Dowdy Jackson, John Taraszka, Y Karen Wang, Michael D Jones, Michael Morrissey, James Deeds and 4 more

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
5.5field-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

70 citing papers in PubMed, 123 citations in OpenAlex.

  1. Biomedicines · 2026
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  15. The Role of Polycomb Group Protein BMI1 in DNA Repair and Genomic Stability.International journal of molecular sciences · 2021
    Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Inhibition of chemotherapy resistant breast cancer stem cells by a ROR1 specific antibody.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article

10 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

14 authors at 1 institution in 1 country.

Dmitri WiederschainOncology Research, Novartis Institutes for BioMedical Research, Cambridge, MA 02139, USA.
Lin Chen
Brett Johnson
Kimberly Bettano
Dowdy Jackson
John Taraszka
Y Karen Wang
Michael D Jones
Michael Morrissey
James Deeds
Rebecca Mosher
Paul Fordjour
Christoph Lengauer
John D Benson
Novartis (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bmi-1 and Mel-18 are structural homologues that belong to the Polycomb group of transcriptional regulators and are believed to stably maintain repression of gene expression by altering the state of chromatin at specific promoters. While a number of clinical and experimental observations have implicated Bmi-1 in human tumorigenesis, the role of Mel-18 in cancer cell growth has not been investigated. We report here that short hairpin RNA-mediated knockdown of either Bmi-1 or Mel-18 in human medulloblastoma DAOY cells results in the inhibition of proliferation, loss of clonogenic survival, anchorage-independent growth, and suppression of tumor formation in nude mice. Furthermore, overexpression of both Bmi-1 and Mel-18 significantly increases the clonogenic survival of Rat1 fibroblasts. In contrast, stable downregulation of Bmi-1 or Mel-18 alone does not affect the growth of normal human WI38 fibroblasts. Proteomics-based characterization of Bmi-1 and Mel-18 protein complexes isolated from cancer cells revealed substantial similarities in their respective compositions. Finally, gene expression analysis identified a number of cancer-relevant pathways that may be controlled by Bmi-1 and Mel-18 and also showed that these Polycomb proteins regulate a set of common gene targets. Taken together, these results suggest that Bmi-1 and Mel-18 may have overlapping functions in cancer cell growth.

Indexed as

Sequence Homology, Amino AcidAnimalsCell DeathCell ProliferationCell SurvivalDNA-Binding ProteinsDown-RegulationFibroblastsGene ExpressionGene Expression ProfilingGene Expression Regulation, NeoplasticHeLa CellsHumansMedulloblastomaMiceNuclear ProteinsBMI1 protein, humanDNA-Binding ProteinsNuclear ProteinsPCGF2 protein, humanPolycomb-Group ProteinsPolycomb Repressive Complex 1Proto-Oncogene ProteinsRepressor ProteinsRNA, Small Interfering

Identifiers

PMID17452456
PMCPMC1951487
OpenAlexW2067933362

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.