Evidence map›Paper›PMID 40809945›Full record

ArticleNAR cancer2025

SETD6 mediates selective interaction and genomic occupancy of BRD4 and MITF in melanoma cells.

Tzofit Elbaz Biton, Michal Feldman, Tomer Davidy, Nili Tickotsky Moskovitz, Liron Levin, Daniel Sevilla, Colin R Goding, Emily Bernstein, Dan Levy

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in NAR cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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

9 authors.

Tzofit Elbaz BitonThe Shraga Segal Department of Microbiology, Immunology and Genetics, Ben-Gurion University of the Negev, P.O.B. 653, Be'er-Sheva 84105, Israel.
Michal FeldmanThe Shraga Segal Department of Microbiology, Immunology and Genetics, Ben-Gurion University of the Negev, P.O.B. 653, Be'er-Sheva 84105, Israel.
Tomer DavidyThe Shraga Segal Department of Microbiology, Immunology and Genetics, Ben-Gurion University of the Negev, P.O.B. 653, Be'er-Sheva 84105, Israel.
Nili Tickotsky MoskovitzBioinformatics Core Facility, Ilse Katz Institute for Nanoscale Science and Technology, Ben-Gurion University of the Negev, P.O.B. 653, Be'er-Sheva 84105, Israel.
Liron LevinBioinformatics Core Facility, Ilse Katz Institute for Nanoscale Science and Technology, Ben-Gurion University of the Negev, P.O.B. 653, Be'er-Sheva 84105, Israel.
Daniel SevillaThe Research Support Laboratories of Ilse Katz Institute for Nano-Science and Technology, Ben-Gurion University of the Negev, P.O.B. 653, Be'er-Sheva 84105, Israel.
Colin R GodingLudwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Headington, Oxford OX3 7DQ, United Kingdom.
Emily BernsteinDepartment of Oncological Sciences, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, United States.
Dan LevyThe Shraga Segal Department of Microbiology, Immunology and Genetics, Ben-Gurion University of the Negev, P.O.B. 653, Be'er-Sheva 84105, Israel.ORCID 0000-0003-0719-0305

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant transcriptional programs mediate malignant transformation of melanoma, the most aggressive form of skin cancer. The lysine methyltransferase SETD6 has been implicated in regulating transcription, cell adhesion, migration, and other processes in various cancers; however its role in melanoma remains unexplored. We recently reported that SETD6 monomethylates the BRD4 at K99 to selectively regulate transcription of genes involved in mRNA (messenger RNA) translation. Here, we observed that BRD4 methylation at K99 by SETD6 occurs in melanoma cells. Knockout of SETD6 or a point mutation at BRD4-K99 disrupts BRD4 genomic occupancy. In addition, we show that SETD6 interacts with MITF, a master transcription factor in melanocytes and melanoma, and influences the genomic distribution of MITF. Mechanistically, we uncover a novel chromatin-localized interaction between BRD4 and MITF in melanoma. Our data suggest that BRD4 binds MITF in melanoma cells and that this interaction is dependent on both SETD6-mediated methylation of BRD4 and MITF acetylation. This chromatin complex plays a pivotal role in selective recruitment of BRD4 and MITF to different genomic loci in melanoma cells.

Indexed as

Histone-Lysine N-MethyltransferaseMelanomaMicrophthalmia-Associated Transcription FactorNuclear ProteinsSkin NeoplasmsTranscription FactorsBromodomain Containing ProteinsCell Cycle ProteinsCell Line, TumorChromatinGene Expression Regulation, NeoplasticHumansMethylationBRD4 protein, humanBromodomain Containing ProteinsCell Cycle ProteinsChromatinHistone-Lysine N-MethyltransferaseMicrophthalmia-Associated Transcription FactorMITF protein, humanNuclear ProteinsTranscription Factors

Identifiers

PMID40809945
PMCPMC12342177

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Registered trials

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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.