Evidence map›Paper›PMID 28785061›Full record

ArticleScientific reports2017

Topotecan is a potent inhibitor of SUMOylation in glioblastoma multiforme and alters both cellular replication and metabolic programming.

Joshua D Bernstock, Daniel Ye, Florian A Gessler, Yang-Ja Lee, Luca Peruzzotti-Jametti, Peter Baumgarten, Kory R Johnson, Dragan Maric, Wei Yang, Donat Kögel and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing 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

28 citing papers in PubMed, 40 citations in OpenAlex.

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  10. The emerging roles of SUMOylation in pulmonary diseases.Molecular medicine (Cambridge, Mass.) · 2023
    Review
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  12. SUMOtherapeutics for Ischemic Stroke.Pharmaceuticals (Basel, Switzerland) · 2023
    Review
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  16. Article
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  19. Current Status of SUMOylation Inhibitors.Current medicinal chemistry · 2021
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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

12 authors at 5 institutions in 3 countries.

Joshua D BernstockStroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA. bernstockjd@ninds.nih.gov.ORCID 0000-0002-7814-3867
Daniel YeStroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0002-5417-3279
Florian A GesslerWellcome Trust-Medical Research Council Stem Cell Institute, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.ORCID 0000-0002-3471-0575
Yang-Ja LeeStroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA.
Luca Peruzzotti-JamettiWellcome Trust-Medical Research Council Stem Cell Institute, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.ORCID 0000-0002-9396-5607
Peter BaumgartenEdinger Institute, Johann Wolfgang Goethe-Universität, Frankfurt am Main, Germany.
Kory R JohnsonBioinformatics Section, Information Technology & Bioinformatics Program, Division of Intramural Research (DIR), (NINDS/NIH), Bethesda, MD, USA.
Dragan MaricFlow Cytometry Core Facility, National Institute of Neurological Disorders and Stroke, National Institutes of Health (NINDS/NIH), Bethesda, MD, USA.
Wei YangDepartment of Anesthesiology, Duke University Medical Center, Durham, NC, USA.ORCID 0000-0001-5719-4393
Donat KögelDepartment of Neurosurgery, Johann Wolfgang Goethe-Universität, Frankfurt am Main, Germany.
Stefano PluchinoWellcome Trust-Medical Research Council Stem Cell Institute, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.ORCID 0000-0002-6267-9472
John M HallenbeckStroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA.
National Institutes of Health · USGoethe University Frankfurt · DEWellcome/MRC Cambridge Stem Cell Institute · GBDuke Medical Center · USOffice of Extramural Research · US

Funding

Medical Research Council MC_PC_12009Wellcome Trust
6 · The paper itself

Abstract

Protein SUMOylation is a dynamic post-translational modification shown to be involved in a diverse set of physiologic processes throughout the cell. SUMOylation has also been shown to play a role in the pathobiology of myriad cancers, one of which is glioblastoma multiforme (GBM). As such, the clinical significance and therapeutic utility offered via the selective control of global SUMOylation is readily apparent. There are, however, relatively few known/effective inhibitors of global SUMO-conjugation. Herein we describe the identification of topotecan as a novel inhibitor of global SUMOylation. We also provide evidence that inhibition of SUMOylation by topotecan is associated with reduced levels of CDK6 and HIF-1α, as well as pronounced changes in cell cycle progression and cellular metabolism, thereby highlighting its putative role as an adjuvant therapy in defined GBM patient populations.

Indexed as

Antineoplastic AgentsBlotting, WesternCell CycleCell ProliferationCyclin-Dependent Kinase 6Enzyme InhibitorsGlioblastomaHumansHypoxia-Inducible Factor 1, alpha SubunitImmunohistochemistrySumoylationTopotecanTumor Cells, CulturedAntineoplastic AgentsCDK6 protein, humanCyclin-Dependent Kinase 6Enzyme InhibitorsHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitTopotecan

Identifiers

PMID28785061
PMCPMC5547153
OpenAlexW2740765687

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.