Evidence map›Paper›PMID 21789792›Full record

ArticleOncotarget2011

c-JUN prevents methylation of p16(INK4a) (and Cdk6): the villain turned bodyguard.

Karoline Kollmann, Gerwin Heller, Veronika Sexl

Open access · hybridAbstract read
In one paragraph

Article in Oncotarget, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

  1. Trial
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  4. CDK4/6 and MAPK-Crosstalk as Opportunity for Cancer Treatment.Pharmaceuticals (Basel, Switzerland) · 2020
    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

3 authors at 2 institutions in 1 country.

Karoline KollmannInstitute of Pharmacology and Toxicology, University of Veterinary Medicine, Vienna, Austria. Karoline. Kollmann@vetmeduni.ac.at
Gerwin Heller
Veronika Sexl
University of Veterinary Medicine Vienna · ATComprehensive Cancer Center Vienna · AT

Funding

Austrian Science Fund FWF P 19723
6 · The paper itself

Abstract

A novel way by which the AP-1 factor c-JUN interferes with tumorigenesis has recently been elucidated [1]. In a model of murine leukemia, c-JUN prevents the epigenetic silencing of the cell cycle kinase CDK6. In the absence of c-JUN, CDK6 is down-regulated and the 5’region of the gene is methylated. Down-regulation of CDK6 results in significantly delayed leukemia formation. Here we show that c-JUN is also involved in protecting the promoter region of the tumor suppressor p16(INK4a), which is consistently methylated over time in c-JUN deficient cells. In cells expressing c-JUN, p16(INK4a) promoter methylation is a less frequent event. Our study unravels a novel mechanism by which the AP-1 factor c-JUN acts as a “bodyguard”,and preventing methylation of a distinct set of genes after oncogenic transformation.

Indexed as

DNA MethylationAnimalsCell Line, TumorCell Transformation, NeoplasticCyclin-Dependent Kinase 6Cyclin-Dependent Kinase Inhibitor p16Disease Models, AnimalDisease ProgressionEpigenesis, GeneticGene Expression Regulation, NeoplasticGene SilencingHumansJNK Mitogen-Activated Protein KinasesLeukemiaMiceMutant ProteinsCyclin-Dependent Kinase 6Cyclin-Dependent Kinase Inhibitor p16JNK Mitogen-Activated Protein KinasesMutant Proteins

Identifiers

PMID21789792
PMCPMC3248190
OpenAlexW1786783872

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.