Evidence map›Paper›PMID 28119527›Full record

ArticleLeukemia2017

RUNX3 is oncogenic in natural killer/T-cell lymphoma and is transcriptionally regulated by MYC.

V Selvarajan, M Osato, G S S Nah, J Yan, T-H Chung, D C-C Voon, Y Ito, M F Ham, M Salto-Tellez, N Shimizu and 4 more

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

Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

42 citing papers in PubMed, 69 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 5 institutions in 4 countries.

V SelvarajanDepartment of Pathology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.ORCID 0000-0002-6017-3902
M OsatoCancer Science Institute of Singapore, National University of Singapore, Singapore.
G S S NahCancer Science Institute of Singapore, National University of Singapore, Singapore.
J YanCancer Science Institute of Singapore, National University of Singapore, Singapore.
T-H ChungCancer Science Institute of Singapore, National University of Singapore, Singapore.
D C-C VoonInstitute for Frontier Science Initiative, Kanazawa University, Japan.
Y ItoCancer Science Institute of Singapore, National University of Singapore, Singapore.
M F HamDepartment of Anatomical Pathology, Faculty of Medicine, University of Indonesia, West Java, Indonesia.
M Salto-TellezCancer Science Institute of Singapore, National University of Singapore, Singapore.
N ShimizuDepartment of Virology, Tokyo Medical and Dental University, Tokyo, Japan.
S-N ChooDepartment of Pathology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
S FanDepartment of Pathology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
W-J ChngCancer Science Institute of Singapore, National University of Singapore, Singapore.
S-B NgDepartment of Pathology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
National University of Singapore · SGKanazawa University · JPQueen's University Belfast · GBTokyo Medical and Dental University · JPUniversity of Indonesia · ID

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RUNX3, runt-domain transcription factor, is a master regulator of gene expression in major developmental pathways. It acts as a tumor suppressor in many cancers but is oncogenic in certain tumors. We observed upregulation of RUNX3 mRNA and protein expression in nasal-type extranodal natural killer (NK)/T-cell lymphoma (NKTL) patient samples and NKTL cell lines compared to normal NK cells. RUNX3 silenced NKTL cells showed increased apoptosis and reduced cell proliferation. Potential binding sites for MYC were identified in the RUNX3 enhancer region. Chromatin immunoprecipitation-quantitative PCR revealed binding activity between MYC and RUNX3. Co-transfection of the MYC expression vector with RUNX3 enhancer reporter plasmid resulted in activation of RUNX3 enhancer indicating that MYC positively regulates RUNX3 transcription in NKTL cell lines. Treatment with a small-molecule MYC inhibitor (JQ1) caused significant downregulation of MYC and RUNX3, leading to apoptosis in NKTL cells. The growth inhibition resulting from depletion of MYC by JQ1 was rescued by ectopic MYC expression. In summary, our study identified RUNX3 overexpression in NKTL with functional oncogenic properties. We further delineate that MYC may be an important upstream driver of RUNX3 upregulation and since MYC is upregulated in NKTL, further study on the employment of MYC inhibition as a therapeutic strategy is warranted.

Indexed as

Gene Expression Regulation, NeoplasticApoptosisAzepinesBinding SitesCell DivisionCell Line, TumorCell Transformation, NeoplasticCore Binding Factor Alpha 3 SubunitEnhancer Elements, GeneticGenes, ReporterGenetic VectorsHumansLymphoma, Extranodal NK-T-CellMolecular Targeted TherapyNose NeoplasmsProtein Interaction MappingAzepinesCore Binding Factor Alpha 3 Subunit(+)-JQ1 compoundMYC protein, humanProto-Oncogene Proteins c-mycRecombinant Fusion ProteinsRNA, Small InterferingRunx3 protein, humanTriazoles

Identifiers

PMID28119527
PMCPMC5629367
OpenAlexW2581423279

What OpenQuestion holds

Textmetadata
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.