Evidence map›Paper›PMID 26853466›Full record

ArticleOncogene2016

HDAC7 inhibition resets STAT3 tumorigenic activity in human glioblastoma independently of EGFR and PTEN: new opportunities for selected targeted therapies.

P Peixoto, A Blomme, B Costanza, R Ronca, S Rezzola, A P Palacios, L Schoysman, S Boutry, N Goffart, O Peulen and 12 more

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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Synthesis and biological evaluation ofJournal of enzyme inhibition and medicinal chemistry · 2024
    Article
  3. HDAC7 promotes ovarian cancer malignancy via AKT/mTOR signalling pathway.Journal of cellular and molecular medicine · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. HDAC7: a promising target in cancer.Frontiers in oncology · 2024
    Review
  8. AKAP12 promotes cancer stem cell-like phenotypes and activates STAT3 in colorectal cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Histone deacetylase inhibitor MPT0B291 suppresses Glioma GrowthInternational journal of biological sciences · 2020
    Article
  15. Article
  16. Article
  17. Article
  18. 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

22 authors at 5 institutions in 4 countries.

P PeixotoMetastasis Research Laboratory, GIGA Cancer, Avenue d'Hopital 3, University of Liège, Liège, Belgium.
A BlommeMetastasis Research Laboratory, GIGA Cancer, Avenue d'Hopital 3, University of Liège, Liège, Belgium.
B CostanzaMetastasis Research Laboratory, GIGA Cancer, Avenue d'Hopital 3, University of Liège, Liège, Belgium.
R RoncaDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
S RezzolaDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
A P PalaciosMetastasis Research Laboratory, GIGA Cancer, Avenue d'Hopital 3, University of Liège, Liège, Belgium.
L SchoysmanDepartment of Radiology, University Hospital Liège, Liège, Belgium.
S BoutryNMR and Molecular Imaging Laboratory, Department of General, Organic and Biomedical Chemistry, University of Mons, Mons, Belgium.
N GoffartGIGA Neurosciences, University of Liège, Liège, Belgium.
O PeulenMetastasis Research Laboratory, GIGA Cancer, Avenue d'Hopital 3, University of Liège, Liège, Belgium.
P MarisMetastasis Research Laboratory, GIGA Cancer, Avenue d'Hopital 3, University of Liège, Liège, Belgium.
E Di ValentinGIGA-Viral Vectors Platform, University of Liège, Liège, Belgium.
V HennequièreMetastasis Research Laboratory, GIGA Cancer, Avenue d'Hopital 3, University of Liège, Liège, Belgium.
E BianchiDepartment of Pathology, University Hospital Liège, Liège, Belgium.
A HenryMetastasis Research Laboratory, GIGA Cancer, Avenue d'Hopital 3, University of Liège, Liège, Belgium.
P MeunierDepartment of Radiology, University Hospital Liège, Liège, Belgium.
B RogisterGIGA Neurosciences, University of Liège, Liège, Belgium.
R N MullerNMR and Molecular Imaging Laboratory, Department of General, Organic and Biomedical Chemistry, University of Mons, Mons, Belgium.
P DelvenneDepartment of Pathology, University Hospital Liège, Liège, Belgium.
A BellahcèneMetastasis Research Laboratory, GIGA Cancer, Avenue d'Hopital 3, University of Liège, Liège, Belgium.
V CastronovoMetastasis Research Laboratory, GIGA Cancer, Avenue d'Hopital 3, University of Liège, Liège, Belgium.
A TurtoiMetastasis Research Laboratory, GIGA Cancer, Avenue d'Hopital 3, University of Liège, Liège, Belgium.
University of Liège · BECentre Hospitalier Universitaire de Liège · BEUniversity of Mons · BEBrescia University · USUniversity of Brescia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To date, the mutational status of EGFR and PTEN has been shown as relevant for favoring pro- or anti-tumor functions of STAT3 in human glioblastoma multiforme (GBM). We have screened genomic data from 154 patients and have identified a strong positive correlation between STAT3 and HDAC7 expression. In the current work we show the existence of a subpopulation of patients overexpressing HDAC7 and STAT3 that has particularly poor clinical outcome. Surprisingly, the somatic mutation rate of both STAT3 and HDAC7 was insignificant in GBM comparing with EGFR, PTEN or TP53. Depletion of HDAC7 in a range of GBM cells induced the expression of tyrosine kinase JAK1 and the tumor suppressor AKAP12. Both proteins synergistically sustained the activity of STAT3 by inducing its phosphorylation (JAK1) and protein expression (AKAP12). In absence of HDAC7, activated STAT3 was responsible for significant imbalance of secreted pro-/anti-angiogenic factors. This inhibited the migration and sprouting of endothelial cells in paracrine fashion in vitro as well as angiogenesis in vivo. In a murine model of GBM, induced HDAC7-silencing decreased the tumor burden by threefold. The current data show for the first time that silencing HDAC7 can reset the tumor suppressor activity of STAT3, independently of the EGFR/PTEN/TP53 background of the GBM. This effect could be exploited to overcome tumor heterogeneity and provide a new rationale behind the development of specific HDAC7 inhibitors for clinical use.

Indexed as

A Kinase Anchor ProteinsAnimalsBrainCell Cycle ProteinsCell Line, TumorErbB ReceptorsGlioblastomaHistone Deacetylase InhibitorsHistone DeacetylasesHumansJanus Kinase 1MaleMiceNeovascularization, PathologicPTEN PhosphohydrolaseSTAT3 Transcription FactorAKAP12 protein, humanA Kinase Anchor ProteinsCell Cycle ProteinsEGFR protein, humanErbB ReceptorsHDAC7 protein, humanHistone Deacetylase InhibitorsHistone DeacetylasesJAK1 protein, humanJanus Kinase 1PTEN PhosphohydrolasePTEN protein, humanSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID26853466
OpenAlexW2254558694

What OpenQuestion holds

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Registered trials

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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.