Evidence map›Paper›PMID 36194562›Full record

ArticlePloS one2022

AT-hook DNA-binding motif-containing protein one knockdown downregulates EWS-FLI1 transcriptional activity in Ewing's sarcoma cells.

Takao Kitagawa, Daiki Kobayashi, Byron Baron, Hajime Okita, Tatsuo Miyamoto, Rie Takai, Durga Paudel, Tohru Ohta, Yoichi Asaoka, Masayuki Tokunaga and 5 more

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

Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.3field-weighted citation impact, top 44% 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

5 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
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

15 authors at 6 institutions in 2 countries.

Takao KitagawaAdvanced Research Promotion Center, Health Sciences University of Hokkaido, Kanazawa, Ishikari-Tobetsu, Hokkaido, Japan.ORCID 0000-0001-7753-827X
Daiki KobayashiDepartment of Omics and Systems Biology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, Japan.ORCID 0000-0003-4131-5220
Byron BaronCenter for Molecular Medicine and Biobanking, University of Malta, Msida, Malta.
Hajime OkitaDivision of Diagnostic Pathology, Keio University School of Medicine, Shinano, Shinjuku-ku, Tokyo, Japan.
Tatsuo MiyamotoDepartment of Molecular and Cellular Physiology, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi, Japan.ORCID 0000-0002-1097-0647
Rie TakaiAdvanced Research Promotion Center, Health Sciences University of Hokkaido, Kanazawa, Ishikari-Tobetsu, Hokkaido, Japan.
Durga PaudelAdvanced Research Promotion Center, Health Sciences University of Hokkaido, Kanazawa, Ishikari-Tobetsu, Hokkaido, Japan.
Tohru OhtaAdvanced Research Promotion Center, Health Sciences University of Hokkaido, Kanazawa, Ishikari-Tobetsu, Hokkaido, Japan.
Yoichi AsaokaDepartment of Systems Biochemistry in Pathology and Regeneration, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi, Japan.
Masayuki TokunagaDepartment of Obstetrics and Gynecology, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi, Japan.
Koji NakagawaAdvanced Research Promotion Center, Health Sciences University of Hokkaido, Kanazawa, Ishikari-Tobetsu, Hokkaido, Japan.
Makoto Furutani-SeikiDepartment of Systems Biochemistry in Pathology and Regeneration, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi, Japan.
Norie ArakiDepartment of Tumor Genetics and Biology, Faculty of Life Sciences, Kumamoto University, Kumamoto-Shi, Kumamoto, Japan.
Yasuhiro KuramitsuAdvanced Research Promotion Center, Health Sciences University of Hokkaido, Kanazawa, Ishikari-Tobetsu, Hokkaido, Japan.
Masanobu KobayashiAdvanced Research Promotion Center, Health Sciences University of Hokkaido, Kanazawa, Ishikari-Tobetsu, Hokkaido, Japan.
Health Sciences University of Hokkaido · JPYamaguchi University · JPKeio University · JPKumamoto University · JPNiigata University · JPUniversity of Malta · MT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ewing's sarcoma is the second most common bone malignancy in children or young adults and is caused by an oncogenic transcription factor by a chromosomal translocation between the EWSR1 gene and the ETS transcription factor family. However, the transcriptional mechanism of EWS-ETS fusion proteins is still unclear. To identify the transcriptional complexes of EWS-ETS fusion transcription factors, we applied a proximal labeling system called BioID in Ewing's sarcoma cells. We identified AHDC1 as a proximal protein of EWS-ETS fusion proteins. AHDC1 knockdown showed a reduced cell growth and transcriptional activity of EWS-FLI1. AHDC1 knockdown also reduced BRD4 and BRG1 protein levels, both known as interacting proteins of EWS-FLI1. Our results suggest that AHDC1 supports cell growth through EWS-FLI1.

Indexed as

Sarcoma, EwingBromodomain Containing ProteinsCell Cycle ProteinsChildDNADNA-Binding ProteinsGene Expression Regulation, NeoplasticHumansNuclear ProteinsOncogene Proteins, FusionProto-Oncogene Protein c-fli-1RNA-Binding Protein EWSTranscription FactorsAHDC1 protein, humanBRD4 protein, humanBromodomain Containing ProteinsCell Cycle ProteinsDNADNA-Binding ProteinsEWS-FLI fusion proteinNuclear ProteinsOncogene Proteins, FusionProto-Oncogene Protein c-fli-1RNA-Binding Protein EWSTranscription Factors

Identifiers

PMID36194562
PMCPMC9531837
OpenAlexW4301374173

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.