Evidence map›Paper›PMID 27604143›Full record

ArticleScientific reports2016

NSD2 contributes to oncogenic RAS-driven transcription in lung cancer cells through long-range epigenetic activation.

Verónica García-Carpizo, Jacinto Sarmentero, Bomie Han, Osvaldo Graña, Sergio Ruiz-Llorente, David G Pisano, Manuel Serrano, Harold B Brooks, Robert M Campbell, Maria J Barrero

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

40 citing papers in PubMed, 55 citations in OpenAlex.

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  17. NSD2 as a Promising Target in Hematological Disorders.International journal of molecular sciences · 2022
    Review
  18. The role of NSD1, NSD2, and NSD3 histone methyltransferases in solid tumors.Cellular and molecular life sciences : CMLS · 2022
    Review
  19. Article
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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

10 authors at 3 institutions in 2 countries.

Verónica García-CarpizoCNIO-Lilly Epigenetics Laboratory, Spanish National Cancer Research Center (CNIO), C/ Melchor Fernández Almagro, 3. 28029 Madrid, Spain.
Jacinto SarmenteroCNIO-Lilly Epigenetics Laboratory, Spanish National Cancer Research Center (CNIO), C/ Melchor Fernández Almagro, 3. 28029 Madrid, Spain.
Bomie HanEli Lilly and Company, 46285 Indianapolis, USA.
Osvaldo GrañaStructural Biology and Biocomputing Program, Spanish National Cancer Research Center (CNIO), C/ Melchor Fernández Almagro, 3. 28029 Madrid, Spain.
Sergio Ruiz-LlorenteCNIO-Lilly Epigenetics Laboratory, Spanish National Cancer Research Center (CNIO), C/ Melchor Fernández Almagro, 3. 28029 Madrid, Spain.
David G PisanoStructural Biology and Biocomputing Program, Spanish National Cancer Research Center (CNIO), C/ Melchor Fernández Almagro, 3. 28029 Madrid, Spain.
Manuel SerranoMolecular Oncology Program, Spanish National Cancer Research Center (CNIO), C/Melchor Fernández Almagro, 3. 28029 Madrid, Spain.
Harold B BrooksEli Lilly and Company, 46285 Indianapolis, USA.
Robert M CampbellEli Lilly and Company, 46285 Indianapolis, USA.
Maria J BarreroCNIO-Lilly Epigenetics Laboratory, Spanish National Cancer Research Center (CNIO), C/ Melchor Fernández Almagro, 3. 28029 Madrid, Spain.
Spanish National Cancer Research Centre · ESCentro de Investigación del Cáncer · ESEli Lilly (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The histone methyltransferase NSD2/WHSC1/MMSET is overexpressed in a number of solid tumors but its contribution to the biology of these tumors is not well understood. Here, we describe that NSD2 contributes to the proliferation of a subset of lung cancer cell lines by supporting oncogenic RAS transcriptional responses. NSD2 knock down combined with MEK or BRD4 inhibitors causes co-operative inhibitory responses on cell growth. However, while MEK and BRD4 inhibitors converge in the downregulation of genes associated with cancer-acquired super-enhancers, NSD2 inhibition affects the expression of clusters of genes embedded in megabase-scale regions marked with H3K36me2 and that contribute to the RAS transcription program. Thus, combinatorial therapies using MEK or BRD4 inhibitors together with NSD2 inhibition are likely to be needed to ensure a more comprehensive inhibition of oncogenic RAS-driven transcription programs in lung cancers with NSD2 overexpression.

Indexed as

Genes, rasAnimalsAzepinesBenzamidesBromodomain Containing ProteinsCell Cycle ProteinsCell Line, TumorCell ProliferationDiphenylamineEnhancer Elements, GeneticEnzyme InhibitorsEpigenesis, GeneticGene ExpressionGene Knockdown TechniquesHistone-Lysine N-MethyltransferaseHistonesAzepinesBenzamidesBRD4 protein, humanBromodomain Containing ProteinsCell Cycle ProteinsDiphenylamineEnzyme InhibitorsHistone-Lysine N-MethyltransferaseHistones(+)-JQ1 compoundMAP Kinase Kinase KinasesmirdametinibNSD2 protein, humanNuclear ProteinsRepressor ProteinsTranscription FactorsTriazoles

Identifiers

PMID27604143
PMCPMC5015087
OpenAlexW2518462838

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.