Evidence map›Paper›PMID 31399646›Full record

ArticleOncogene2019

Spermidine/spermine N1-acetyltransferase 1 is a gene-specific transcriptional regulator that drives brain tumor aggressiveness.

Vijay S Thakur, Brittany Aguila, Adina Brett-Morris, Chad J Creighton, Scott M Welford

Abstract read
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 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

34 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Article
  3. Mechanisms of Protection Against Oxidative Stress During Hibernation.International journal of molecular sciences · 2026
    Review
  4. Article
  5. Article
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  10. Targeting MELK in tumor cells and tumor microenvironment: from function and mechanism to therapeutic application.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  11. Article
  12. Article
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  14. Review
  15. Article
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  18. Review
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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 3 institutions in 1 country.

Vijay S ThakurDepartment of Radiation Oncology, Miller School of Medicine, University of Miami, Miami, FL, 33136, USA.
Brittany AguilaDepartment of Biochemistry, Case Western Reserve University, Cleveland, OH, 44106, USA.
Adina Brett-MorrisDepartment of Pharmacology, Case Western Reserve University, Cleveland, OH, 44106, USA.
Chad J CreightonDan L. Duncan Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX, 77030, USA.
Scott M WelfordDepartment of Radiation Oncology, Miller School of Medicine, University of Miami, Miami, FL, 33136, USA. scott.welford@med.miami.edu.ORCID http://orcid.org/0000-0002-9579-4223
Case Western Reserve University · USUniversity of Miami · USBaylor College of Medicine · US

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9M
Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
Polyamine Catabolism and Therapeutic Resistance in Glioblastoma MultiformeR01CA187053 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI WELFORD, SCOTT MICHAEL · 2015 to 2025
$3.5M
NCI NIH HHS P30 CA125123NCI NIH HHS R01 CA187053NIDDK NIH HHS P30 DK058404
6 · The paper itself

Abstract

Spermidine/spermine N1-acetyltransferase 1 (SAT1), the rate-limiting enzyme in polyamine catabolism, has broad regulatory roles due to near ubiquitous polyamine binding. We describe a novel function of SAT1 as a gene-specific transcriptional regulator through local polyamine acetylation. SAT1 expression is elevated in aggressive brain tumors and promotes resistance to radiotherapy. Expression profiling in glioma cells identified SAT1 target genes that distinguish high- and low-grade tumors, in support of the prognostic utility of SAT1 expression. We further discovered mechanisms of SAT1-driven tumor aggressiveness through promotion of expression of both DNA damage response pathways as well as cell cycle regulatory genes. Mechanistically, SAT1 associates specifically with the promoter of the MELK gene, which functionally controls other SAT1 targets, and leads biologically to maintenance of neurosphere stemness in conjunction with FOXM1 and EZH2. CRISPR knockin mutants demonstrate the essentiality of the polyamine acetyltransferase activity of SAT1 for its function as a transcriptional regulator. Together, the data demonstrate that gene-specific polyamine removal is a major transcriptional regulatory mechanism active in high-grade gliomas that drives poor outcomes.

Indexed as

Transcription, GeneticAcetyltransferasesBrain NeoplasmsChromatinDiamine N-AcetyltransferaseEnhancer of Zeste Homolog 2 ProteinGliomaHumansNeoplastic Stem CellsProtein Serine-Threonine KinasesAcetyltransferasesChromatinDiamine N-AcetyltransferaseEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanMELK protein, humanProtein Serine-Threonine Kinases

Identifiers

PMID31399646
PMCPMC6786946
OpenAlexW2967227564

What OpenQuestion holds

Textmetadata
LicenceTDM
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.