Evidence map›Paper›PMID 29945296›Full record

ArticleCancer science2018

EWS-FLI1 regulates a transcriptional program in cooperation with Foxq1 in mouse Ewing sarcoma.

Rikuka Shimizu, Miwa Tanaka, Shuichi Tsutsumi, Hiroyuki Aburatani, Yukari Yamazaki, Mizuki Homme, Yoshimasa Kitagawa, Takuro Nakamura

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

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  7. EWS::FLI1 and HOXD13 Control Tumor Cell Plasticity in Ewing Sarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 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

8 authors at 3 institutions in 1 country.

Rikuka ShimizuDivision of Carcinogenesis, The Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
Miwa TanakaDivision of Carcinogenesis, The Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
Shuichi TsutsumiGenome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan.
Hiroyuki AburataniGenome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan.
Yukari YamazakiDivision of Carcinogenesis, The Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
Mizuki HommeDivision of Carcinogenesis, The Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
Yoshimasa KitagawaDepartment of Oral Diagnosis and Medicine, Faculty of Dental Medicine, Hokkaido University, Sapporo, Japan.
Takuro NakamuraDivision of Carcinogenesis, The Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.ORCID http://orcid.org/0000-0002-0419-7547
Japanese Foundation For Cancer Research · JPSapporo University · JPThe University of Tokyo · JP

Funding

Japan Society for the Promotion of Science 16K07131Japan Society for the Promotion of Science 26250029Mitsubishi Foundation 29133
6 · The paper itself

Abstract

EWS-FLI1 constitutes an oncogenic transcription factor that plays key roles in Ewing sarcoma development and maintenance. We have recently succeeded in generating an ex vivo mouse model for Ewing sarcoma by introducing EWS-FLI1 into embryonic osteochondrogenic progenitors. The model well recapitulates the biological characteristics, small round cell morphology, and gene expression profiles of human Ewing sarcoma. Here, we clarified the global DNA binding properties of EWS-FLI1 in mouse Ewing sarcoma. GGAA microsatellites were found to serve as binding sites of EWS-FLI1 albeit with less frequency than that in human Ewing sarcoma; moreover, genomic distribution was not conserved between human and mouse. Nevertheless, EWS-FLI1 binding sites within GGAA microsatellites were frequently associated with the histone H3K27Ac enhancer mark, suggesting that EWS-FLI1 could affect global gene expression by binding its target sites. In particular, the Fox transcription factor binding motif was frequently observed within EWS-FLI1 peaks and Foxq1 was identified as the cooperative partner that interacts with the EWS portion of EWS-FLI1. Trib1 and Nrg1 were demonstrated as target genes that are co-regulated by EWS-FLI1 and Foxq1, and are important for cell proliferation and survival of Ewing sarcoma. Collectively, our findings present novel aspects of EWS-FLI1 function as well as the importance of GGAA microsatellites.

Indexed as

AnimalsApoptosisBinding SitesCell CycleCell Line, TumorCell ProliferationChondrogenesisDisease Models, AnimalDNA-Binding ProteinsEmbryonic Stem CellsEpithelial-Mesenchymal TransitionForkhead Transcription FactorsGene Expression Regulation, NeoplasticHistonesHumansIntracellular Signaling Peptides and ProteinsDNA-Binding ProteinsEWS-FLI fusion proteinForkhead Transcription FactorsFoxq1 protein, mouseHistonesIntracellular Signaling Peptides and ProteinsNeuregulin-1Nrg1 protein, mouseOncogene Proteins, FusionProtein Serine-Threonine KinasesProto-Oncogene Protein c-fli-1RNA-Binding Protein EWSRNA, Small InterferingTrib1 protein, mouseEwing sarcomaEWS-FLI1Foxq1GGAA microsatelliteTrib1

Identifiers

PMID29945296
PMCPMC6125457
OpenAlexW2811413097

What OpenQuestion holds

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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 OpenQuestion graph.