Evidence map›Paper›PMID 33497366›Full record

ArticleJCI insight2021

Tristetraprolin expression by keratinocytes protects against skin carcinogenesis.

Assiya Assabban, Ingrid Dubois-Vedrenne, Laurye Van Maele, Rosalba Salcedo, Brittany L Snyder, Lecong Zhou, Abdulkader Azouz, Bérengère de Toeuf, Gaëlle Lapouge, Caroline La and 11 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

9 citing papers in PubMed, 13 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

21 authors at 5 institutions in 2 countries.

Assiya AssabbanInstitute for Medical Immunology, ULB Center for Research in Immunology, and ULB Center for Cancer Research, Université Libre de Bruxelles, Gosselies, Belgium.
Ingrid Dubois-VedrenneInstitute for Medical Immunology, ULB Center for Research in Immunology, and ULB Center for Cancer Research, Université Libre de Bruxelles, Gosselies, Belgium.
Laurye Van MaeleInstitute for Medical Immunology, ULB Center for Research in Immunology, and ULB Center for Cancer Research, Université Libre de Bruxelles, Gosselies, Belgium.
Rosalba SalcedoCancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland, USA.
Brittany L SnyderSignal Transduction Laboratory and.
Lecong ZhouIntegrative Bioinformatics Support Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA.
Abdulkader AzouzInstitute for Medical Immunology, ULB Center for Research in Immunology, and ULB Center for Cancer Research, Université Libre de Bruxelles, Gosselies, Belgium.
Bérengère de ToeufLaboratoire de Biologie Moléculaire du Gène, ULB Center for Research in Immunology, Université Libre de Bruxelles, Gosselies, Belgium.
Gaëlle LapougeLaboratory of Stem Cells and Cancer, WELBIO, and ULB Cancer Research Center, Université Libre de Bruxelles, Brussels, Belgium.
Caroline LaInstitute for Medical Immunology, ULB Center for Research in Immunology, and ULB Center for Cancer Research, Université Libre de Bruxelles, Gosselies, Belgium.
Maxime MelchiorInstitute for Medical Immunology, ULB Center for Research in Immunology, and ULB Center for Cancer Research, Université Libre de Bruxelles, Gosselies, Belgium.
Muriel NguyenInstitute for Medical Immunology, ULB Center for Research in Immunology, and ULB Center for Cancer Research, Université Libre de Bruxelles, Gosselies, Belgium.
Séverine ThomasInstitute for Medical Immunology, ULB Center for Research in Immunology, and ULB Center for Cancer Research, Université Libre de Bruxelles, Gosselies, Belgium.
Si Fan WuLaboratoire de Biologie Moléculaire du Gène, ULB Center for Research in Immunology, Université Libre de Bruxelles, Gosselies, Belgium.
Wenqian HuDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, New York, USA.
Véronique KruysLaboratoire de Biologie Moléculaire du Gène, ULB Center for Research in Immunology, Université Libre de Bruxelles, Gosselies, Belgium.
Cédric BlanpainLaboratory of Stem Cells and Cancer, WELBIO, and ULB Cancer Research Center, Université Libre de Bruxelles, Brussels, Belgium.
Giorgio TrinchieriCancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland, USA.
Cyril GueydanLaboratoire de Biologie Moléculaire du Gène, ULB Center for Research in Immunology, Université Libre de Bruxelles, Gosselies, Belgium.
Perry J BlackshearSignal Transduction Laboratory and.
Stanislas GorielyInstitute for Medical Immunology, ULB Center for Research in Immunology, and ULB Center for Cancer Research, Université Libre de Bruxelles, Gosselies, Belgium.
Université Libre de Bruxelles · BENational Cancer Institute · USDuke Medical Center · USMayo Clinic · USNational Institute of Environmental Health Sciences · US

Funding

TTP and related proteins in the regulation of gene expressionZIAES090080 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BLACKSHEAR, PERRY J · 2009 to 2025
$52.6M
Role of inflammation, innate resistance, and immunity in carcinogenesis.ZIABC010793 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI TRINCHIERI, GIORGIO · 2009 to 2025
$16.8M
6 · The paper itself

Abstract

Cancer is caused primarily by genomic alterations resulting in deregulation of gene regulatory circuits in key growth, apoptosis, or DNA repair pathways. Multiple genes associated with the initiation and development of tumors are also regulated at the level of mRNA decay, through the recruitment of RNA-binding proteins to AU-rich elements (AREs) located in their 3'-untranslated regions. One of these ARE-binding proteins, tristetraprolin (TTP; encoded by Zfp36), is consistently dysregulated in many human malignancies. Herein, using regulated overexpression or conditional ablation in the context of cutaneous chemical carcinogenesis, we show that TTP represents a critical regulator of skin tumorigenesis. We provide evidence that TTP controlled both tumor-associated inflammation and key oncogenic pathways in neoplastic epidermal cells. We identify Areg as a direct target of TTP in keratinocytes and show that EGFR signaling potentially contributed to exacerbated tumor formation. Finally, single-cell RNA-Seq analysis indicated that ZFP36 was downregulated in human malignant keratinocytes. We conclude that TTP expression by epidermal cells played a major role in the control of skin tumorigenesis.

Indexed as

3' Untranslated RegionsAnimalsAU Rich ElementsCarcinogenesisDisease Models, AnimalDown-RegulationErbB ReceptorsGene Regulatory NetworksHumansInflammationKeratinocytesMiceMice, Inbred C57BLRNA-Binding ProteinsRNA, MessengerRNA Stability3' Untranslated RegionsEGFR protein, humanErbB ReceptorsRNA-Binding ProteinsRNA, MessengerTristetraprolinZFP36 protein, humanCytokinesInflammationMouse modelsOncologySkin cancer

Identifiers

PMID33497366
PMCPMC8021119
OpenAlexW3124438342

What OpenQuestion holds

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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.