Evidence map›Paper›PMID 26527316›Full record

ArticleOncotarget2015

IRAK1 is a novel DEK transcriptional target and is essential for head and neck cancer cell survival.

Allie K Adams, Lyndsey C Bolanos, Phillip J Dexheimer, Rebekah A Karns, Bruce J Aronow, Kakajan Komurov, Anil G Jegga, Keith A Casper, Yash J Patil, Keith M Wilson and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 41 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

12 authors at 2 institutions in 1 country.

Allie K AdamsDivision of Oncology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Lyndsey C BolanosDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Phillip J DexheimerDivision of Biomedical Informatics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Rebekah A KarnsDivision of Biomedical Informatics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Bruce J AronowDivision of Biomedical Informatics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Kakajan KomurovDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Anil G JeggaDivision of Biomedical Informatics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Keith A CasperDepartment of Otolaryngology, Head and Neck Surgery, University of Cincinnati, Cincinnati, OH, USA.
Yash J PatilDepartment of Otolaryngology, Head and Neck Surgery, University of Cincinnati, Cincinnati, OH, USA.
Keith M WilsonDepartment of Otolaryngology, Head and Neck Surgery, University of Cincinnati, Cincinnati, OH, USA.
Daniel T StarczynowskiDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Susanne I WellsDivision of Oncology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Cincinnati Children's Hospital Medical Center · USUniversity of Cincinnati · US

Funding

Stem Cell/Organoid and Genome Editing CoreP30DK078392 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Alexander Miethke · 2007 to 2026
$24.4M
ENVIRONMETAL CARCINOGENESIS AND MUTAGENESIST32ES007250 · NIEHS · UNIVERSITY OF CINCINNATI · PI MILLER, WILLIAM E · 1988 to 2024
$11.9M
ROLE OF ANGPTL4, AN ANGIOGENIC MEDIATOR, IN ARTHRITISP30AR047363 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI FLICK, MATTHEW J. · 2001 to 2015
$9.2M
Training Program in Cancer TherapeuticsT32CA117846 · NCI · UNIVERSITY OF CINCINNATI · PI PRICE, CAROLYN M, TAKIAR, VINITA · 2006 to 2022
$6.5M
Cincinnati Center for Excellence in Molecular HematologyP30DK090971 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI ZHENG, YI · 2010 to 2015
$4.0M
Role and Regulaton of the Human DEK Proto-OncogeneR01CA116316 · NCI · CINCINNATI CHILDRENS HOSP MED CTR · PI WELLS, SUSANNE I · 2006 to 2016
$2.9M
Identification and characterization of genes in del(5q) myelodysplastic syndromeR01HL111103 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI STARCZYNOWSKI, DANIEL · 2012 to 2016
$1.9M
Role of TRAF6 in Myelodysplastic SyndromesR01HL114582 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI STARCZYNOWSKI, DANIEL · 2014 to 2016
$1.2M
Molecular Pathogenesis of MDSR01DK102759 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI STARCZYNOWSKI, DANIEL · 2014 to 2016
$701k
NCI NIH HHS R01 CA116316NCI NIH HHS T32 CA117846NHLBI NIH HHS R01 HL111103NHLBI NIH HHS R01 HL114582NIAMS NIH HHS AR-47363NIAMS NIH HHS P30 AR047363NIDDK NIH HHS DK78392NIDDK NIH HHS DK90971NIDDK NIH HHS P30 DK078392NIDDK NIH HHS P30 DK090971NIDDK NIH HHS R01 DK102759NIEHS NIH HHS T32 ES007250NIEHS NIH HHS T32ES007250
6 · The paper itself

Abstract

The chromatin-binding DEK protein was recently reported to promote the growth of HPV+ and HPV- head and neck squamous cell carcinomas (HNSCCs). Relevant cellular and molecular mechanism(s) controlled by DEK in HNSCC remain poorly understood. While DEK is known to regulate specific transcriptional targets, global DEK-dependent gene networks in HNSCC are unknown. To identify DEK transcriptional signatures we performed RNA-Sequencing (RNA-Seq) in HNSCC cell lines that were either proficient or deficient for DEK. Bioinformatic analyses and subsequent validation revealed that IRAK1, a regulator of inflammatory signaling, and IRAK1-dependent regulatory networks were significantly repressed upon DEK knockdown in HNSCC. According to TCGA data, 14% of HNSCC specimens overexpressed IRAK1, thus supporting possible oncogenic functions. Furthermore, genetic or pharmacologic inhibition of IRAK1 in HNSCC cell lines was sufficient to attenuate downstream signaling such as ERK1/2 and to induce HNSCC cell death by apoptosis. Finally, targeting DEK and IRAK1 simultaneously enhanced cell death as compared to targeting either alone. Our findings reveal that IRAK1 promotes cell survival and is an attractive therapeutic target in HNSCC cells. Thus, we propose a model wherein IRAK1 stimulates tumor signaling and phenotypes both independently and in conjunction with DEK.

Indexed as

Blotting, WesternCarcinoma, Squamous CellCell SurvivalChromosomal Proteins, Non-HistoneFlow CytometryGene Expression Regulation, NeoplasticGene Knockdown TechniquesGene Regulatory NetworksHead and Neck NeoplasmsHigh-Throughput Nucleotide SequencingHumansImmunohistochemistryImmunoprecipitationInterleukin-1 Receptor-Associated KinasesOligonucleotide Array Sequence AnalysisOncogene ProteinsChromosomal Proteins, Non-HistoneDEK protein, humanInterleukin-1 Receptor-Associated KinasesIRAK1 protein, humanOncogene ProteinsPoly-ADP-Ribose Binding ProteinsDEKHNSCCHPVIRAK1RNA-Seq

Identifiers

PMID26527316
PMCPMC4791239
OpenAlexW2253394189

What OpenQuestion holds

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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.