Evidence map›Paper›PMID 41275493›Full record

ArticleCell reports2025

MITF, TFEB, and TFE3 drive distinct adaptive gene expression programs and immune infiltration in melanoma.

Diogo Dias, Erica Oliveira, Román Martí-Díaz, Sarah Andrews, Ana Chocarro-Calvo, Alice Bellini, Laura Mosteo, Yurena Vivas García, Jagat Chauhan, Linxin Li and 9 more

Abstract read
In one paragraph

Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors.

Diogo DiasLudwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Old Road Campus Research Building, Old Road Campus, Headington, Oxford OX3 7DQ, UK.
Erica OliveiraLudwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Old Road Campus Research Building, Old Road Campus, Headington, Oxford OX3 7DQ, UK.
Román Martí-DíazDepartment of Biochemistry and Molecular Biology A, School of Biology, University of Murcia, Instituto Murciano de Investigación Biosanitaria (IMIB), 30120 Murcia, Spain.
Sarah AndrewsLudwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Old Road Campus Research Building, Old Road Campus, Headington, Oxford OX3 7DQ, UK.
Ana Chocarro-CalvoArea of Physiology, Faculty Health Sciences, University Rey Juan Carlos, Alcorcón, 28922 Madrid, Spain.
Alice BelliniLudwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Old Road Campus Research Building, Old Road Campus, Headington, Oxford OX3 7DQ, UK.
Laura MosteoLudwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Old Road Campus Research Building, Old Road Campus, Headington, Oxford OX3 7DQ, UK.
Yurena Vivas GarcíaLudwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Old Road Campus Research Building, Old Road Campus, Headington, Oxford OX3 7DQ, UK.
Jagat ChauhanLudwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Old Road Campus Research Building, Old Road Campus, Headington, Oxford OX3 7DQ, UK.
Linxin LiLudwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Old Road Campus Research Building, Old Road Campus, Headington, Oxford OX3 7DQ, UK.
José Manuel García-MartinezArea of Physiology, Faculty Health Sciences, University Rey Juan Carlos, Alcorcón, 28922 Madrid, Spain.
José Neptuno Rodriguez-LópezDepartment of Biochemistry and Molecular Biology A, School of Biology, University of Murcia, Instituto Murciano de Investigación Biosanitaria (IMIB), 30120 Murcia, Spain.
Silvya Stuchi Maria-EnglerDepartment of Clinical and Toxicological Analysis School of Pharmaceutical Sciences, University of São Paulo, São Paulo 05508-000, Brazil.
Colin KennyDepartment of Surgery, Carver College of Medicine, University of Iowa, Iowa City, IA, USA; Holden Comprehensive Cancer Center, Carver College of Medicine, University of Iowa, Iowa City, IA, USA.
Javier Martínez-UserosArea of Physiology, Faculty Health Sciences, University Rey Juan Carlos, Alcorcón, 28922 Madrid, Spain.
Custodia García-JiménezArea of Physiology, Faculty Health Sciences, University Rey Juan Carlos, Alcorcón, 28922 Madrid, Spain.
Luis Sanchez-Del-CampoDepartment of Biochemistry and Molecular Biology A, School of Biology, University of Murcia, Instituto Murciano de Investigación Biosanitaria (IMIB), 30120 Murcia, Spain.
Pakavarin LouphrasitthipholLudwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Old Road Campus Research Building, Old Road Campus, Headington, Oxford OX3 7DQ, UK. Electronic address: pakavarin.louphrasitthiphol@ludwig.ox.ac.uk.
Colin R GodingLudwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Old Road Campus Research Building, Old Road Campus, Headington, Oxford OX3 7DQ, UK. Electronic address: colin.goding@ludwig.ox.ac.uk.

Funding

The integrated stress response and the microenvironment in melanoma progressionR01CA268597 · NCI · UNIVERSITY OF PENNSYLVANIA · PI Colin Goding, Constantinos Koumenis · 2022 to 2026
$2.0M
NCI NIH HHS PO1 CA128814-06A1NCI NIH HHS R01 CA268597
6 · The paper itself

Abstract

Cells can contain multiple related transcription factors targeting the same sequences, leading to potential regulatory cooperativity, redundancy, competition, or temporally regulated factor exchange. Yet, the differential biological functions of co-targeting transcription factors are poorly understood. In melanoma, three highly related transcription factors are co-expressed: the mammalian target of rapamycin complex 1 (mTORC1)-regulated TFEB and TFE3 (both key effectors of a wide range of metabolic and microenvironmental cues assumed to perform similar functions) and the microphthalmia-associated transcription factor (MITF), which controls melanoma phenotypic identity. Here, we reveal the functional specialization of MITF, TFE3, and TFEB and their impact on melanoma progression. Notably, although all bind the same sequences, each regulates different and frequently opposing gene expression programs to coordinate differentiation, metabolism, and protein synthesis and qualitatively and quantitatively impacts tumor immune infiltration. The results uncover a hierarchical cascade whereby microenvironmental stresses, including glucose limitation, lead MITF, TFEB, and TFE3 to drive distinct biologically important transcription programs that underpin phenotypic transitions in cancer.

Indexed as

Basic Helix-Loop-Helix Leucine Zipper Transcription FactorsGene Expression Regulation, NeoplasticMelanomaMicrophthalmia-Associated Transcription FactorAnimalsCell Line, TumorHumansMiceBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsMicrophthalmia-Associated Transcription FactorMITF protein, humanTFE3 protein, humanTFEB protein, humanCP: cancerCP: genomicsmelanomamelanoma gene regulationMITFTFE3TFEBtumor immune infiltration

Identifiers

PMID41275493
PMCPMC12828906

What Socratic 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 Socratic graph.