Evidence map›Paper›PMID 26930713›Full record

ArticleOncotarget2016

Histone deacetylase 9 regulates breast cancer cell proliferation and the response to histone deacetylase inhibitors.

Marion Lapierre, Aurélien Linares, Mathieu Dalvai, Céline Duraffourd, Sandrine Bonnet, Abdelhay Boulahtouf, Carmen Rodriguez, Stéphan Jalaguier, Said Assou, Beatrice Orsetti and 6 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

35 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. SOX9: an important factor in regulating breast cancer.European journal of medical research · 2025
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Association ofmedRxiv : the preprint server for health sciences · 2023
    Article
  12. The functional role of circular RNAs in the pathogenesis of retinoblastoma: a new potential biomarker and therapeutic target?Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
  13. Insights into the transition of ductal carcinomaCancer biology & medicine · 2022
    Article
  14. Article
  15. Differential molecular mechanistic behavior of HDACs in cancer progression.Medical oncology (Northwood, London, England) · 2022
    Review
  16. Article
  17. Review
  18. Review
  19. 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

16 authors at 6 institutions in 1 country.

Marion LapierreIRCM, Institut de Recherche en Cancérologie de Montpellier, Montpellier, France.
Aurélien LinaresIRCM, Institut de Recherche en Cancérologie de Montpellier, Montpellier, France.
Mathieu DalvaiUniversité de Toulouse, UPS, Laboratoire de Biologie Moléculaire Eucaryote (LBME), Toulouse, France.
Céline DuraffourdLaboratoire de Biologie Cellulaire, CHU Arnaud de Villeneuve, Montpellier, France.
Sandrine BonnetIRCM, Institut de Recherche en Cancérologie de Montpellier, Montpellier, France.
Abdelhay BoulahtoufIRCM, Institut de Recherche en Cancérologie de Montpellier, Montpellier, France.
Carmen RodriguezIRCM, Institut de Recherche en Cancérologie de Montpellier, Montpellier, France.
Stéphan JalaguierIRCM, Institut de Recherche en Cancérologie de Montpellier, Montpellier, France.
Said AssouUniversité Montpellier, Montpellier, France.
Beatrice OrsettiIRCM, Institut de Recherche en Cancérologie de Montpellier, Montpellier, France.
Patrick BalaguerIRCM, Institut de Recherche en Cancérologie de Montpellier, Montpellier, France.
Thierry MaudelondeLaboratoire de Biologie Cellulaire, CHU Arnaud de Villeneuve, Montpellier, France.
Philippe BlacheIRCM, Institut de Recherche en Cancérologie de Montpellier, Montpellier, France.
Kerstin BystrickyUniversité de Toulouse, UPS, Laboratoire de Biologie Moléculaire Eucaryote (LBME), Toulouse, France.
Nathalie BoulleIRCM, Institut de Recherche en Cancérologie de Montpellier, Montpellier, France.
Vincent CavaillèsIRCM, Institut de Recherche en Cancérologie de Montpellier, Montpellier, France.
Université de Montpellier · FRInserm · FRInstitut de Recherche en Cancérologie de Montpellier · FRHôpital Arnaud de Villeneuve · FRLaboratoire de Biologie Moléculaire des Eucaryotes · FRUniversité Fédérale de Toulouse Midi-Pyrénées · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone lysine acetylation is an epigenetic mark regulated by histone acetyltransferases and histone deacetylases (HDAC) which plays an important role in tumorigenesis. In this study, we observed a strong overexpression of class IIa HDAC9, at the mRNA and protein levels, in the most aggressive human breast cancer cell lines (i.e. in basal breast cancer cells vs luminal ones or in malignant vs begnin MCF10A breast epithelial cell lines). HDAC9 overexpression was associated with higher rates of gene transcription and increased epigenetic marks on the HDAC9 promoter. Ectopic expression of HDAC9 in MCF7 luminal breast cancer cells led to an increase in cell proliferation and to a decrease in apoptosis. These effects were associated with a deregulated expression of several genes controlled by HDAC inhibitors such as CDKN1A, BAX and TNFRSF10A. Inversely, knock-down of HDAC9 expression in MDA-MB436 basal breast cancer cells reduced cell proliferation. Moreover, high HDAC9 expression decreased the efficacy of HDAC inhibitors to reduce cell proliferation and to regulate CDKN1A gene expression. Interestingly, the gene encoding the transcription factor SOX9 was identified by a global transcriptomic approach as an HDAC9 target gene. In stably transfected MCF7 cells, SOX9 silencing significantly decreased HDAC9 mitogenic activity. Finally, in a large panel of breast cancer biopsies, HDAC9 expression was significantly increased in tumors of the basal subtype, correlated with SOX9 expression and associated with poor prognosis. Altogether, these results indicate that HDAC9 is a key factor involved in mammary carcinogenesis and in the response to HDAC inhibitors.

Indexed as

ApoptosisBlotting, WesternBreast NeoplasmsCell LineCell Line, TumorCell ProliferationFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHistone Deacetylase InhibitorsHistone DeacetylasesHumansMCF-7 CellsMicroscopy, FluorescenceRepressor ProteinsRNA InterferenceHDAC9 protein, humanHistone Deacetylase InhibitorsHistone DeacetylasesRepressor ProteinsSOX9 protein, humanSOX9 Transcription Factorbreast cancerHDAC9HDAC inhibitorshistone deacetylaseSOX9

Identifiers

PMID26930713
PMCPMC4991412
OpenAlexW2324761201

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.