Evidence map›Paper›PMID 20807887›Full record

ArticleBlood2010

TEL-AML1 regulation of survivin and apoptosis via miRNA-494 and miRNA-320a.

Christofer Diakos, Sheng Zhong, Yuanyuan Xiao, Mi Zhou, Gisele M Vasconcelos, Gerd Krapf, Ru-Fang Yeh, Shichun Zheng, Michelle Kang, John K Wiencke and 3 more

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00015587 (Chemical Exposures and Leukemia Risks and Childhood Leukemia and Environmental Exposure), which is not on this map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing 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.

NCT00015587 completednot on this map

Chemical Exposures and Leukemia Risks and Childhood Leukemia and Environmental Exposure

TypeobservationalSponsorNational Institute of Environmental Health Sciences (NIEHS)Ran1995 to 2016Enrolled3,523ConditionsLeukemia, Acute Myelocytic Leukemia, Acute Lymphoblastic Leukemia, Acute Myelogenous Leukemia
3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 73 citations in OpenAlex.

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  18. miR-494 suppresses tumor growth of epithelial ovarian carcinoma by targeting IGF1R.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
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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

13 authors at 3 institutions in 3 countries.

Christofer DiakosLaboratory for Molecular Epidemiology, University of California, San Francisco, San Francisco, CA, USA.
Sheng Zhong
Yuanyuan Xiao
Mi Zhou
Gisele M Vasconcelos
Gerd Krapf
Ru-Fang Yeh
Shichun Zheng
Michelle Kang
John K Wiencke
Maria S Pombo-de-Oliveira
Renate Panzer-Grümayer
Joseph L Wiemels
University of California, San Francisco · USSt Anna Children's Hospital · ATInstituto Nacional do Câncer · BR

Funding

BACKTRACKING TRANSLOCATIONS IN CHILDHOOD LEUKEMIAR01CA089032 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WIEMELS, JOSEPH LEO · 2001 to 2006
$1.6M
DNA methylation in the development of pediatric leukemiasR03CA137829 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ZHONG, SHENG · 2009 to 2010
$155k
NCI NIH HHS R01 CA089032NCI NIH HHS R01-CA89032NCI NIH HHS R03 CA137829NCI NIH HHS R03-CA137829
6 · The paper itself

Abstract

There is increasing evidence that miRNA and transcription factors interact in an instructive fashion in normal and malignant hematopoiesis. We explored the impact of TEL-AML1 (ETV6-RUNX1), the most common fusion protein in childhood leukemia, on miRNA expression and the leukemic phenotype. Using RNA interference, miRNA expression arrays, and quantitative polymerase chain reaction, we identified miRNA-494 and miRNA-320a to be up-regulated upon TEL-AML1 silencing independently of TEL expression. Chromatin immunoprecipitation analysis identified miRNA-494 as a direct miRNA target of the fusion protein TEL-AML1. Using bioinformatic analysis as well as functional luciferase experiments, we demonstrate that survivin is a target of the 2 miRNAs. miRNA-494 and miRNA-320a were introduced to the cells by transfection and survivin expression determined by Western blot analysis. These miRNAs blocked survivin expression and resulted in apoptosis in a similar manner as TEL-AML1 silencing by itself; this silencing was also shown to be Dicer-dependent. miRNAs-494 and -320a are expressed at lower levels in TEL-AML1+ leukemias compared with immunophenotype-matched nonTEL-AML1 acute lymphoblastic leukemia subtypes, and within TEL-AML1+ leukemias their expression is correlated to survivin levels. In summary our data suggest that TEL-AML1 might exert its antiapoptotic action at least in part by suppressing miRNA-494 and miRNA-320a, lowering their expression causing enhanced survivin expression.

Indexed as

Gene Expression Regulation, NeoplasticAdolescentApoptosisBlotting, WesternCell Line, TumorChildChild, PreschoolChromatin ImmunoprecipitationCore Binding Factor Alpha 2 SubunitETS Translocation Variant 6 ProteinGene ExpressionHumansInhibitor of Apoptosis ProteinsMicroRNAsMicrotubule-Associated ProteinsOligonucleotide Array Sequence AnalysisBIRC5 protein, humanCore Binding Factor Alpha 2 SubunitETS Translocation Variant 6 ProteinInhibitor of Apoptosis ProteinsMicroRNAsMicrotubule-Associated ProteinsOncogene Proteins, FusionRNA, MessengerSurvivinTEL-AML1 fusion protein

Identifiers

PMID20807887
PMCPMC3265147
OpenAlexW2068368007

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.