Evidence map›Paper›PMID 28119061›Full record

ArticleEBioMedicine2017

NFIB Mediates BRN2 Driven Melanoma Cell Migration and Invasion Through Regulation of EZH2 and MITF.

Mitchell E Fane, Yash Chhabra, David E J Hollingsworth, Jacinta L Simmons, Loredana Spoerri, Tae Gyu Oh, Jagat Chauhan, Toby Chin, Lachlan Harris, Tracey J Harvey and 7 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EBioMedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

52 citing papers in PubMed, 107 citations in OpenAlex.

  1. Nuclear Factor I-B Delays Liver Fibrosis by Inhibiting Chemokine Ligand 5 Transcription.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  14. Transcriptional Regulation ofInternational journal of molecular sciences · 2022
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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

17 authors at 5 institutions in 2 countries.

Mitchell E FaneThe School of Biomedical Sciences, The University of Queensland, Brisbane, QLD 4072, Australia; School of Biomedical Sciences, Institute of Health and Biomedical Innovation at the Translational Research Institute, Queensland University of Technology, Woolloongabba, QLD 4102, Australia.
Yash ChhabraThe School of Biomedical Sciences, The University of Queensland, Brisbane, QLD 4072, Australia; School of Biomedical Sciences, Institute of Health and Biomedical Innovation at the Translational Research Institute, Queensland University of Technology, Woolloongabba, QLD 4102, Australia.
David E J HollingsworthThe School of Biomedical Sciences, The University of Queensland, Brisbane, QLD 4072, Australia.
Jacinta L SimmonsCancer Drug Mechanisms Group, Department of Cell and Molecular Biology, QIMR Berghofer Medical Research Institute, Herston, Queensland 4006, Australia.
Loredana SpoerriThe University of Queensland Diamantina Institute, The University of Queensland, Brisbane, QLD, Australia.
Tae Gyu OhInstitute for Molecular Bioscience, The University of Queensland, St. Lucia, QLD 4072, Australia.
Jagat ChauhanLudwig Institute for Cancer Research, Nuffield Department of Medicine, University of Oxford, Headington, Oxford OX3 7DQ, UK.
Toby ChinThe School of Biomedical Sciences, The University of Queensland, Brisbane, QLD 4072, Australia.
Lachlan HarrisThe School of Biomedical Sciences, The University of Queensland, Brisbane, QLD 4072, Australia.
Tracey J HarveyThe School of Biomedical Sciences, The University of Queensland, Brisbane, QLD 4072, Australia.
George E O MuscatInstitute for Molecular Bioscience, The University of Queensland, St. Lucia, QLD 4072, Australia.
Colin R GodingLudwig Institute for Cancer Research, Nuffield Department of Medicine, University of Oxford, Headington, Oxford OX3 7DQ, UK.
Richard A SturmDermatology Research Centre, The University of Queensland, School of Medicine, Translational Research Institute, Brisbane, QLD 4102, Australia.
Nikolas K HaassThe University of Queensland Diamantina Institute, The University of Queensland, Brisbane, QLD, Australia.
Glen M BoyleCancer Drug Mechanisms Group, Department of Cell and Molecular Biology, QIMR Berghofer Medical Research Institute, Herston, Queensland 4006, Australia.
Michael PiperThe School of Biomedical Sciences, The University of Queensland, Brisbane, QLD 4072, Australia; Queensland Brain Institute, The University of Queensland, Brisbane, QLD 4072, Australia.
Aaron G SmithSchool of Biomedical Sciences, Institute of Health and Biomedical Innovation at the Translational Research Institute, Queensland University of Technology, Woolloongabba, QLD 4102, Australia; Dermatology Research Centre, The University of Queensland, School of Medicine, Translational Research Institute, Brisbane, QLD 4102, Australia. Electronic address: a260.smith@qut.edu.au.
University of Queensland · AUQIMR Berghofer Medical Research Institute · AULudwig Cancer Research · GBTranslational Research Institute · AUUniversity of Oxford · GB

Funding

Tumor Assessment CoreP01CA128814 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI SMITH, JEFFREY W · 2009 to 2020
$19.1M
NCI NIH HHS P01 CA128814
6 · The paper itself

Abstract

While invasion and metastasis of tumour cells are the principle factor responsible for cancer related deaths, the mechanisms governing the process remain poorly defined. Moreover, phenotypic divergence of sub-populations of tumour cells is known to underpin alternative behaviors linked to tumour progression such as proliferation, survival and invasion. In the context of melanoma, heterogeneity between two transcription factors, BRN2 and MITF, has been associated with phenotypic switching between predominantly invasive and proliferative behaviors respectively. Epigenetic changes, in response to external cues, have been proposed to underpin this process, however the mechanism by which the phenotypic switch occurs is unclear. Here we report the identification of the NFIB transcription factor as a novel downstream effector of BRN2 function in melanoma cells linked to the migratory and invasive characteristics of these cells. Furthermore, the function of NFIB appears to drive an invasive phenotype through an epigenetic mechanism achieved via the upregulation of the polycomb group protein EZH2. A notable target of NFIB mediated up-regulation of EZH2 is decreased MITF expression, which further promotes a less proliferative, more invasive phenotype. Together our data reveal that NFIB has the ability to promote dynamic changes in the chromatin state of melanoma cells to facilitate migration, invasion and metastasis.

Indexed as

AnimalsBlotting, WesternCell Line, TumorCell MovementEnhancer of Zeste Homolog 2 ProteinGene Expression Regulation, NeoplasticHomeodomain ProteinsHumansMaleMelanomaMice, Inbred BALB CMice, KnockoutMicrophthalmia-Associated Transcription FactorMicroscopy, FluorescenceNeoplasm InvasivenessNFI Transcription FactorsEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanHomeodomain ProteinsMicrophthalmia-Associated Transcription FactorMITF protein, humanNFIB protein, humanNFI Transcription FactorsPOU Domain Factorstranscription factor Brn-2BRN2EpigeneticInvasionMelanomaMetastasisNFIB

Identifiers

PMID28119061
PMCPMC5474438
OpenAlexW2574813995

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.