Evidence map›Paper›PMID 31375747›Full record

ArticleOncogene2019

HDAC7 regulates histone 3 lysine 27 acetylation and transcriptional activity at super-enhancer-associated genes in breast cancer stem cells.

Corrado Caslini, Sunhwa Hong, Yuguang J Ban, Xi S Chen, Tan A Ince

Open access · hybridAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

72 citing papers in PubMed, 125 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. H3K27ac Is Essential for Human Naive Pluripotency Modulated by m6A-Driven EP300 Expression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  11. Article
  12. HDAC7 influences ER-⍺ transcription via NCoR-HDAC3 dissociation.Biochimica et biophysica acta. Proteins and proteomics · 2025
    Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. HDAC7 promotes ovarian cancer malignancy via AKT/mTOR signalling pathway.Journal of cellular and molecular medicine · 2024
    Article
  20. Super-enhancer omics in stem cell.Molecular cancer · 2024
    Review

12 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

5 authors at 1 institution in 2 countries.

Corrado CasliniSylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Biomedical Research Building, Miami, FL, 33136, USA. ccaslini@med.miami.edu.
Sunhwa HongSylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Biomedical Research Building, Miami, FL, 33136, USA.
Yuguang J BanSylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Biomedical Research Building, Miami, FL, 33136, USA.ORCID http://orcid.org/0000-0002-2874-0647
Xi S ChenSylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Biomedical Research Building, Miami, FL, 33136, USA.
Tan A InceSylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Biomedical Research Building, Miami, FL, 33136, USA. TInce@med.miami.edu.
University of Miami · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chromatin regulation through histone modifications plays an essential role in coordinated expression of multiple genes. Alterations in chromatin induced by histone modifiers and readers regulate critical transcriptional programs involved in both normal development and tumor differentiation. Recently, we identified that histone deacetylases HDAC1 and HDAC7 are necessary to maintain cancer stem cells (CSCs) in both breast and ovarian tumors. Here, we sought to investigate the CSC-specific function of HDAC1 and HDAC7 mechanistically by using a stem-like breast cancer (BrCa) cell model BPLER and matched nonstem tumor cell (nsTC)-like HMLER, along with conventional BrCa cell lines with different CSC enrichment levels. We found that HDAC1 and HDAC3 inhibition or knockdown results in HDAC7 downregulation, which is associated with a decrease in histone 3 lysine 27 acetylation (H3K27ac) at transcription start sites (TSS) and super-enhancers (SEs) prominently in stem-like BrCa cells. Importantly, these changes in chromatin landscape also correlate with the repression of many SE-associated oncogenes, including c-MYC, CD44, CDKN1B, SLUG, VDR, SMAD3, VEGFA, and XBP1. In stem-like BrCa cells, HDAC7 binds near TSS and to SEs of these oncogenes where it appears to contribute to both H3K27ac and transcriptional regulation. These results suggest that HDAC7 inactivation, directly or through inhibition of HDAC1 and HDAC3, can result in the inhibition of the CSC phenotype by downregulating multiple SE-associated oncogenes. The CSC selective nature of this mechanism and the prospect of inhibiting multiple oncogenes simultaneously makes development of HDAC7 specific inhibitors a compelling objective.

Indexed as

Enhancer Elements, GeneticTranscription, GeneticAcetylationBenzamidesBreast NeoplasmsDown-RegulationFemaleGene Knockdown TechniquesHistone Deacetylase 1Histone Deacetylase 3Histone Deacetylase InhibitorsHistone DeacetylasesHistonesHumansLysineNeoplastic Stem CellsBenzamidesentinostatHDAC1 protein, humanHDAC7 protein, humanHistone Deacetylase 1Histone Deacetylase 3Histone Deacetylase InhibitorsHistone DeacetylasesHistonesLysinePyridinesTranscription Factors

Identifiers

PMID31375747
OpenAlexW2966048051

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.