Evidence mapPaperPMID 39282450Full record

ArticlebioRxiv : the preprint server for biology2024

The small MAF transcription factor MAFG co-opts MITF to promote melanoma progression.

Olga Vera, Michael Martinez, Zulaida Soto-Vargas, Kaizhen Wang, Xiaonan Xu, Sara Ruiz-Buceta, Nicol Mecozzi, Manon Chadourne, Benjamin Posorske, Ariana Angarita and 11 more

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

21 authors.

Olga VeraDepartment of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida 33612, USA.ORCID 0000-0002-1878-4945
Michael MartinezDepartment of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida 33612, USA.
Zulaida Soto-VargasDepartment of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida 33612, USA.ORCID 0000-0002-3174-4104
Kaizhen WangDepartment of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida 33612, USA.ORCID 0000-0001-6033-7041
Xiaonan XuDepartment of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida 33612, USA.ORCID 0000-0002-7366-580X
Sara Ruiz-BucetaBiomarkers and Experimental Therapeutics in Cancer, IdiPAZ, 28046 Madrid, Spain.
Nicol MecozziDepartment of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida 33612, USA.ORCID 0000-0001-6161-5074
Manon ChadourneDepartment of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida 33612, USA.
Benjamin PosorskeDepartment of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida 33612, USA.ORCID 0009-0003-7022-5547
Ariana AngaritaDepartment of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida 33612, USA.
Ilah BokDepartment of Cell Biology and Physiology, Washington University, St. Louis, MO 63110, USA.ORCID 0000-0001-8958-5161
Qian LiuCancer Biology PhD Program, University of South Florida, Tampa, FL 33612, USA.
Harini MurikipudiDepartment of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida 33612, USA.
Yumi KimDepartment of Metabolism and Physiology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA.ORCID 0000-0001-8815-3121
Jane L MessinaDepartment of Pathology, H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL 33612, USA.ORCID 0000-0002-0332-0224
Kenneth Y TsaiDepartment of Tumor Microenvironment and Metastasis, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA.ORCID 0000-0001-5325-212X
Michael B MajorDepartment of Cell Biology and Physiology, Washington University, St. Louis, MO 63110, USA.ORCID 0000-0002-6753-8513
Eric K LauDepartment of Tumor Microenvironment and Metastasis, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA.ORCID 0000-0003-3005-3421
Xiaoqing YuDepartment of Biostatistics and Bioinformatics, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida 33612, USA.ORCID 0000-0003-4585-9372
Inmaculada Ibanez-de-CaceresBiomarkers and Experimental Therapeutics in Cancer, IdiPAZ, 28046 Madrid, Spain.ORCID 0000-0001-9805-8486
Florian A KarrethDepartment of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida 33612, USA.ORCID 0000-0002-2350-9809

Funding

Tissue CoreP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · 1998 to 2025
$32.8M
Mechanisms and Targeted Therapy of NRF2-high Esophageal Squamous Cell CarcinomaR01CA244236 · CORIELL INSTITUTE FOR MEDICAL RESEARCH · 2025 to 2025
$618k
Chromosome 1q ceRNAs in Melanoma Progression and MetastasisR01CA259046 · H. LEE MOFFITT CANCER CTR & RES INST · 2025 to 2025
$531k
Molecular Oncology Training GrantT32CA113275 · WASHINGTON UNIVERSITY · 2025 to 2025
$363k
NCI NIH HHS P30 CA076292NCI NIH HHS R01 CA244236NCI NIH HHS R01 CA259046NCI NIH HHS R21 CA256141NCI NIH HHS T32 CA113275
6 · The paper itself

Abstract

Transcription factor deregulation potently drives melanoma progression by dynamically and reversibly controlling gene expression programs. We previously identified the small MAF family transcription factor MAFG as a putative driver of melanoma progression, prompting an in-depth evaluation of its role in melanoma. MAFG expression increases with human melanoma stages and ectopic MAFG expression enhances the malignant behavior of human melanoma cells in vitro, xenograft models, and genetic mouse models of spontaneous melanoma. Moreover, MAFG induces a melanoma phenotype switch from a melanocytic state to a more dedifferentiated state. Mechanistically, MAFG interacts with the lineage transcription factor MITF which is required for the pro-tumorigenic effects of MAFG. MAFG and MITF co-occupy numerous genomic sites and MAFG overexpression influences the expression of genes harboring binding sites for the MAFG~MITF complex. These results establish MAFG as a potent driver of melanomagenesis through dimerization with MITF and uncover an unappreciated mechanism of MITF regulation.

Indexed as

MAFGmelanomaMITFmouse modelphenotype switchingtranscription factor

Identifiers

PMID39282450
PMCPMC11398417

What Socratic holds

Textmetadata
LicenceCC BY-NC
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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 Socratic graph.