Evidence map›Paper›PMID 27132511›Full record

ArticleOncogene2016

Tumor suppressor SET9 guides the epigenetic plasticity of breast cancer cells and serves as an early-stage biomarker for predicting metastasis.

M F Montenegro, L Sánchez-Del-Campo, R González-Guerrero, E Martínez-Barba, A Piñero-Madrona, J Cabezas-Herrera, J N Rodríguez-López

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 40 citations in OpenAlex.

  1. Trial
  2. Review
  3. Lysine and arginine methylation of transcription factors.Cellular and molecular life sciences : CMLS · 2024
    Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. [Research Progress of Role and Mechanism of SETD7 in Tumor Occurrence 
and Progression].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2023
    Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. METTL3/YTHDF2 mJournal of cellular and molecular medicine · 2020
    Article
  20. 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

7 authors at 3 institutions in 2 countries.

M F MontenegroDepartment of Biochemistry and Molecular Biology A, School of Biology, University of Murcia, Instituto Murciano de Investigación Biosanitaria (IMIB), Murcia, Spain.
L Sánchez-Del-CampoLudwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Headington, Oxford, UK.
R González-GuerreroDepartment of Biochemistry and Molecular Biology A, School of Biology, University of Murcia, Instituto Murciano de Investigación Biosanitaria (IMIB), Murcia, Spain.
E Martínez-BarbaDepartment of Pathology, University Hospital Virgen de la Arrixaca, IMIB, Murcia, Spain.
A Piñero-MadronaDepartment of Surgery, University Hospital Virgen de la Arrixaca, IMIB, Murcia, Spain.
J Cabezas-HerreraMolecular Therapy and Biomarkers Research Group, University Hospital Virgen de la Arrixaca, IMIB, Murcia, Spain.
J N Rodríguez-LópezDepartment of Biochemistry and Molecular Biology A, School of Biology, University of Murcia, Instituto Murciano de Investigación Biosanitaria (IMIB), Murcia, Spain.
Universidad de Murcia · ESInstituto Murciano de Investigación Biosanitaria · ESUniversity of Oxford · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During the course of cancer progression, neoplastic cells undergo dynamic and reversible transitions between multiple phenotypic states, and this plasticity is enabled by underlying shifts in epigenetic regulation. Our results identified a negative feedback loop in which SET9 controls DNA methyltransferase-1 protein stability, which represses the transcriptional activity of the SET9 promoter in coordination with Snail. The modulation of SET9 expression in breast cancer cells revealed a connection with E2F1 and the silencing of SET9 was sufficient to complete an epigenetic program that favored epithelial-mesenchymal transition and the generation of cancer stem cells, indicating that SET9 plays a role in modulating breast cancer metastasis. SET9 expression levels were significantly higher in samples from patients with pathological complete remission than in samples from patients with disease recurrence, which indicates that SET9 acts as a tumor suppressor in breast cancer and that its expression may serve as a prognostic marker for malignancy.

Indexed as

Biomarkers, TumorEpigenesis, GeneticGene Expression Regulation, NeoplasticGenes, Tumor SuppressorAnimalsBreast NeoplasmsCell Line, TumorCluster AnalysisDisease Models, AnimalDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesEpithelial-Mesenchymal TransitionFemaleFollow-Up StudiesGene Expression ProfilingHistone-Lysine N-MethyltransferaseBiomarkers, TumorDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesHistone-Lysine N-MethyltransferaseSETD7 protein, humanSnail Family Transcription Factors

Identifiers

PMID27132511
OpenAlexW2347181220

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.