Evidence map›Paper›PMID 29308302›Full record

ArticleOncoimmunology

Glioma-induced SIRT1-dependent activation of hMOF histone H4 lysine 16 acetyltransferase in microglia promotes a tumor supporting phenotype.

Dalel Saidi, Mathilde Cheray, Ahmed M Osman, Vassilis Stratoulias, Olle R Lindberg, Xianli Shen, Klas Blomgren, Bertrand Joseph

Open access · goldAbstract read
In one paragraph

Article in Oncoimmunology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-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

20 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
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  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Microglia and Brain Macrophages as Drivers of Glioma Progression.International journal of molecular sciences · 2022
    Review
  12. Review
  13. NADSignal transduction and targeted therapy · 2020
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Epigenetics Control Microglia Plasticity.Frontiers in cellular neuroscience · 2018
    Review
  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

8 authors at 2 institutions in 1 country.

Dalel SaidiInstitute of Environmental Medicine, Toxicology Unit, Karolinska Institutet, Stockholm, Sweden.
Mathilde CherayInstitute of Environmental Medicine, Toxicology Unit, Karolinska Institutet, Stockholm, Sweden.
Ahmed M OsmanDepartment of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden.
Vassilis StratouliasInstitute of Environmental Medicine, Toxicology Unit, Karolinska Institutet, Stockholm, Sweden.
Olle R LindbergInstitute of Environmental Medicine, Toxicology Unit, Karolinska Institutet, Stockholm, Sweden.
Xianli ShenDepartment of Oncology-Pathology, Cancer Centrum Karolinska, Karolinska Institutet, Stockholm, Sweden.
Klas BlomgrenDepartment of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden.
Bertrand JosephInstitute of Environmental Medicine, Toxicology Unit, Karolinska Institutet, Stockholm, Sweden.
Karolinska Institutet · SEKarolinska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High-grade gliomas are malignant aggressive primary brain tumors with limited therapeutic options, and dismal prognosis for patients. Microglia, the resident immune cells of the brain, are recruited and reprogrammed into tumor-supporting cells by glioma cells, which in turn positively influence tumor expansion and infiltration into surrounding brain tissues. Here, we report that glioma-induced microglia conversion is coupled to an increase of histone H4 lysine 16 (H4K16) acetylation level in microglia, through increased nuclear localization of the deacetylase SIRT1, which in turn results in deacetylation of the H4K16 acetyltransferase hMOF and its recruitment to the chromatin at promoter regions of microglial target genes. Furthermore, we demonstrate that manipulation of the microglial H4K16 acetylation level, taking advantage of the intrinsic H4K16 deacetylase or acetyltransferase activities of SIRT1 and hMOF, respectively, modulated the tumor-supporting function of microglia. This study provides evidence that post-translational modifications of histones and the histone-modifying enzymes controlling them, such as H4K16 acetylation regulated by hMOF and SIRT1, are part of the microglial pro-tumoral activation pathway initiated by glioma cancer cells and represent potentially novel therapeutic targets.

Indexed as

gliomaH4K16 acetylationhMOF (MYST1/KAT8)microgliaSIRT1

Identifiers

PMID29308302
PMCPMC5749650
OpenAlexW2757644079

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.