Evidence map›Paper›PMID 31378787›Full record

ArticleCell death & disease2019

C-Jun drives melanoma progression in PTEN wild type melanoma cells.

Melanie Kappelmann-Fenzl, Claudia Gebhard, Alexander O Matthies, Silke Kuphal, Michael Rehli, Anja Katrin Bosserhoff

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed, 43 citations in OpenAlex.

  1. GTP biosynthesis is a therapeutic vulnerability in Rac1-mutant melanoma.bioRxiv : the preprint server for biology · 2026
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  6. Zoological research · 2025
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  9. Jun, an Oncological Foe or Friend?International journal of molecular sciences · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. HDAC2 Is Involved in the Regulation of BRN3A in Melanocytes and Melanoma.International journal of molecular sciences · 2022
    Article
  15. Article
  16. Article
  17. 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

6 authors at 4 institutions in 1 country.

Melanie Kappelmann-FenzlInstitute of Biochemistry (Emil-Fischer Center), Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany.
Claudia GebhardDepartment of Internal Medicine III, University Hospital Regensburg, Regensburg, Germany.
Alexander O MatthiesInstitute of Biochemistry (Emil-Fischer Center), Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany.
Silke KuphalInstitute of Biochemistry (Emil-Fischer Center), Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany.
Michael RehliDepartment of Internal Medicine III, University Hospital Regensburg, Regensburg, Germany.
Anja Katrin BosserhoffInstitute of Biochemistry (Emil-Fischer Center), Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany. anja.bosserhoff@fau.de.
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEUniversity Hospital Regensburg · DEComprehensive Cancer Center Erlangen · DEDeggendorf Institute of Technology · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Due to the critical impact of active AP-1 transcription factors in melanoma, it is important to define their target genes and to identify and ultimately inhibit oncogenic signals. Here we mapped the genome-wide occupancy of the AP-1 family member c-Jun in different melanoma cells and correlated AP-1 binding with transcriptome data to detect genes in melanoma regulated by c-Jun. Our analysis shows that c-Jun supports the malignant phenotype by deregulating genes in cancer-relevant signaling pathways, such as mitogen-activated protein kinase (MAPK) and phosphatidylinositol-3-kinase (PI3K) pathways. Moreover, we demonstrate that the importance of c-Jun depends on melanoma stage and mutation status of the tumor suppressor PTEN. Our study reveals that activation of c-Jun overrules the tumor suppressive effect of PTEN in early melanoma development. These findings help to understand the relevance of c-Jun within cancer pathways in different melanoma cell types, especially in relation to MAPK and PI3K pathways, which are commonly deregulated in melanomas. Consequently, targeting c-Jun in PTEN

Indexed as

Disease ProgressionCell Line, TumorCell MovementCell ProliferationGene Knockdown TechniquesHumansMelanomaMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-junPTEN PhosphohydrolaseSignal TransductionSkin NeoplasmsTranscription Factor AP-1TransfectionMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-junPTEN PhosphohydrolasePTEN protein, humanTranscription Factor AP-1

Identifiers

PMID31378787
PMCPMC6680049
OpenAlexW2966657471

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.