Evidence map›Paper›PMID 27050748›Full record

ArticleCancer biology & therapy2016

Specific c-Jun target genes in malignant melanoma.

Patrick Schummer, Silke Kuphal, Lily Vardimon, Anja K Bosserhoff, Melanie Kappelmann

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2016. 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
0.9field-weighted citation impact, top 24% 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, 27 citations in OpenAlex.

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  11. Review
  12. DGKA Provides Platinum Resistance in Ovarian Cancer Through Activation of c-JUN-WEE1 Signaling.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020
    Article
  13. Article
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  15. Article
  16. Review
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 2 institutions in 2 countries.

Patrick Schummera Institute of Biochemistry (Emil-Fischer Center), Friedrich-Alexander University Erlangen-Nürnberg , Erlangen , Germany.
Silke Kuphala Institute of Biochemistry (Emil-Fischer Center), Friedrich-Alexander University Erlangen-Nürnberg , Erlangen , Germany.
Lily Vardimonb Department of Biochemistry and Molecular Biology , Tel Aviv University , Israel.
Anja K Bosserhoffa Institute of Biochemistry (Emil-Fischer Center), Friedrich-Alexander University Erlangen-Nürnberg , Erlangen , Germany.
Melanie Kappelmanna Institute of Biochemistry (Emil-Fischer Center), Friedrich-Alexander University Erlangen-Nürnberg , Erlangen , Germany.
Friedrich-Alexander-Universität Erlangen-Nürnberg · DETel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A fundamental event in the development and progression of malignant melanoma is the de-regulation of cancer-relevant transcription factors. We recently showed that c-Jun is a main regulator of melanoma progression and, thus, is the most important member of the AP-1 transcription factor family in this disease. Surprisingly, no cancer-related specific c-Jun target genes in melanoma were described in the literature, so far. Therefore, we focused on pre-existing ChIP-Seq data (Encyclopedia of DNA Elements) of 3 different non-melanoma cell lines to screen direct c-Jun target genes. Here, a specific c-Jun antibody to immunoprecipitate the associated promoter DNA was used. Consequently, we identified 44 direct c-Jun targets and a detailed analysis of 6 selected genes confirmed their deregulation in malignant melanoma. The identified genes were differentially regulated comparing 4 melanoma cell lines and normal human melanocytes and we confirmed their c-Jun dependency. Direct interaction between c-Jun and the promoter/enhancer regions of the identified genes was confirmed by us via ChIP experiments. Interestingly, we revealed that the direct regulation of target gene expression via c-Jun can be independent of the existence of the classical AP-1 (5´-TGA(C/G)TCA-3´) consensus sequence allowing for the subsequent down- or up-regulation of the expression of these cancer-relevant genes. In summary, the results of this study indicate that c-Jun plays a crucial role in the development and progression of malignant melanoma via direct regulation of cancer-relevant target genes and that inhibition of direct c-Jun targets through inhibition of c-Jun is a potential novel therapeutic option for treatment of malignant melanoma.

Indexed as

Cell Line, TumorHumansMelanomaProto-Oncogene Proteins c-junProto-Oncogene Proteins c-junAP-1ChIP-SeqChromatin-immunoprecipitation (ChIP)c-Junmalignant melanomaregulatory mechanismstranscription factors

Identifiers

PMID27050748
PMCPMC4910930
OpenAlexW2334920121

What OpenQuestion holds

Textmetadata
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.