Evidence map›Paper›PMID 36494864›Full record

ArticleGenome biology2022

New roles for AP-1/JUNB in cell cycle control and tumorigenic cell invasion via regulation of cyclin E1 and TGF-β2.

Beatriz Pérez-Benavente, Alihamze Fathinajafabadi, Lorena de la Fuente, Carolina Gandía, Arantxa Martínez-Férriz, José Miguel Pardo-Sánchez, Lara Milián, Ana Conesa, Octavio A Romero, Julián Carretero and 4 more

Open access · goldAbstract read
In one paragraph

Article in Genome biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 39 citations in OpenAlex.

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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

14 authors at 6 institutions in 4 countries.

Beatriz Pérez-Benavente *Centro de Investigación Príncipe Felipe, Valencia, Spain.
Alihamze Fathinajafabadi *Centro de Investigación Príncipe Felipe, Valencia, Spain.
Lorena de la FuenteCentro de Investigación Príncipe Felipe, Valencia, Spain.
Carolina GandíaCentro de Investigación Príncipe Felipe, Valencia, Spain.
Arantxa Martínez-FérrizCentro de Investigación Príncipe Felipe, Valencia, Spain.
José Miguel Pardo-SánchezCentro de Investigación Príncipe Felipe, Valencia, Spain.
Lara MiliánDepartment of Pathology, Faculty of Medicine and Dentistry, Universitat de València, Valencia, Spain.
Ana ConesaSpanish National Research Council, Institute for Integrative Systems Biology, Paterna, Valencia, Spain.
Octavio A RomeroCancer Genetics Group, Josep Carreras Leukaemia Research Institute (IJC), Badalona, Barcelona, Spain.
Julián CarreteroDepartament de Fisiologia, Facultat de Farmacia, Universitat de València, Burjassot, Valencia, Spain.
Rune MatthiesenComputational and Experimental Biology Group, NOVA Medical School-Research, Faculdade de Ciências Médicas, Universidade NOVA de Lisboa, Lisbon, Portugal.
Isabelle Jariel-Encontre *Institut de Génétique Moléculaire de Montpellier, University of Montpellier, CNRS, Montpellier, France.
Marc Piechaczyk *Institut de Génétique Moléculaire de Montpellier, University of Montpellier, CNRS, Montpellier, France.
Rosa FarràsCentro de Investigación Príncipe Felipe, Valencia, Spain. rfarras@cipf.es.ORCID 0000-0003-4931-1494
Centro de Investigacion Principe Felipe · ESCentre National de la Recherche Scientifique · FRUniversitat de València · ESJosep Carreras Leukaemia Research Institute · ESParc Científic de la Universitat de València · ESUniversidade Nova de Lisboa · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundJUNB transcription factor contributes to the formation of the ubiquitous transcriptional complex AP-1 involved in the control of many physiological and disease-associated functions. The roles of JUNB in the control of cell division and tumorigenic processes are acknowledged but still unclear.

resultsHere, we report the results of combined transcriptomic, genomic, and functional studies showing that JUNB promotes cell cycle progression via induction of cyclin E1 and repression of transforming growth factor (TGF)-β2 genes. We also show that high levels of JUNB switch the response of TGF-β2 stimulation from an antiproliferative to a pro-invasive one, induce endogenous TGF-β2 production by promoting TGF-β2 mRNA translation, and enhance tumor growth and metastasis in mice. Moreover, tumor genomic data indicate that JUNB amplification associates with poor prognosis in breast and ovarian cancer patients.

conclusionsOur results reveal novel functions for JUNB in cell proliferation and tumor aggressiveness through regulation of cyclin E1 and TGF-β2 expression, which might be exploited for cancer prognosis and therapy.

Indexed as

NeoplasmsTransforming Growth Factor beta2AnimalsCarcinogenesisCell Cycle CheckpointsCell DivisionMiceTranscription Factor AP-1Transcription FactorsJunB protein, mouseTranscription Factor AP-1Transcription FactorsTransforming Growth Factor beta2AP-1/JUNBCancer progressionCell cycleChIP-seqEpithelial to mesenchymal transitionTranscriptome

Identifiers

PMID36494864
PMCPMC9733061
OpenAlexW4311673453

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.