Evidence map›Paper›PMID 22179826›Full record

ArticleOncogene2012

p27Kip1 represses transcription by direct interaction with p130/E2F4 at the promoters of target genes.

R Pippa, L Espinosa, G Gundem, R García-Escudero, A Dominguez, S Orlando, E Gallastegui, C Saiz, A Besson, M J Pujol and 4 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

48 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. p27International journal of molecular sciences · 2022
    Article
  7. Article
  8. Article
  9. Article
  10. p27Cells · 2021
    Review
  11. Review
  12. Article
  13. Stimulation of c-Jun/AP-1-Activity by the Cell Cycle Inhibitor p57Frontiers in cell and developmental biology · 2021
    Article
  14. Regulation of p27Biomolecules · 2020
    Review
  15. Article
  16. Review
  17. p27 transcriptionally coregulates cJun to drive programs of tumor progression.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  18. Article
  19. Role of p27Oncotarget · 2018
    Review
  20. p27Oncotarget · 2018
    Article
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 7 institutions in 2 countries.

R PippaDepartment of Cell Biology, Immunology and Neurosciences, University of Barcelona, IDIBAPS, and Institut Municipal d' Investigacions Mèdiques-Hospital del Mar, Barcelona, Spain.
L Espinosa
G Gundem
R García-Escudero
A Dominguez
S Orlando
E Gallastegui
C Saiz
A Besson
M J Pujol
N López-Bigas
J M Paramio
A Bigas
O Bachs
Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas · ESUniversitat de Barcelona · ESConsorci Institut D'Investigacions Biomediques August Pi I Sunyer · ESHospital del Mar Research Institute · ESInserm · FRInstitució Catalana de Recerca i Estudis Avançats · ESPompeu Fabra University · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cyclin-cdk (cyclin-dependent kinase) inhibitor p27Kip1 (p27) has a crucial negative role on cell cycle progression. In addition to its classical role as a cyclin-cdk inhibitor, it also performs cyclin-cdk-independent functions as the regulation of cytoskeleton rearrangements and cell motility. p27 deficiency has been associated with tumor aggressiveness and poor clinical outcome, although the mechanisms underlying this participation still remain elusive. We report here a new cellular function of p27 as a transcriptional regulator in association with p130/E2F4 complexes that could be relevant for tumorigenesis. We observed that p27 associates with specific promoters of genes involved in important cellular functions as processing and splicing of RNA, mitochondrial organization and respiration, translation and cell cycle. On these promoters p27 co-localizes with p130, E2F4 and co-repressors as histone deacetylases (HDACs) and mSIN3A. p27 co-immunoprecipitates with these proteins and by affinity chromatography, we demonstrated a direct interaction of p27 with p130 and E2F4 through its carboxyl-half. We have also shown that p130 recruits p27 on the promoters, and there p27 is needed for the subsequent recruitment of HDACs and mSIN3A. Expression microarrays and luciferase assays revealed that p27 behaves as transcriptional repressor of these p27-target genes (p27-TGs). Finally, in human tumors, we established a correlation with overexpression of p27-TGs and poor survival. Thus, this new function of p27 as a transcriptional repressor could have a role in the major aggressiveness of tumors with low levels of p27.

Indexed as

Gene Expression Regulation, NeoplasticPromoter Regions, GeneticTranscription, GeneticAnimalsCo-Repressor ProteinsCyclin-Dependent Kinase Inhibitor p27E2F4 Transcription FactorGene ExpressionHumansMiceModels, BiologicalNeoplasmsNIH 3T3 CellsPrognosisProtein BindingRetinoblastoma-Like Protein p130Co-Repressor ProteinsCyclin-Dependent Kinase Inhibitor p27E2F4 Transcription FactorRetinoblastoma-Like Protein p130

Identifiers

PMID22179826
OpenAlexW1976369107

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.