Evidence map›Paper›PMID 26580398›Full record

ArticlePloS one2015

A Double Negative Loop Comprising ETV6/RUNX1 and MIR181A1 Contributes to Differentiation Block in t(12;21)-Positive Acute Lymphoblastic Leukemia.

Yung-Li Yang, Ching-Tzu Yen, Chen-Hsueh Pai, Hsuan-Yu Chen, Sung-Liang Yu, Chien-Yu Lin, Chung-Yi Hu, Shiann-Tarng Jou, Dong-Tsamn Lin, Shu-Rung Lin and 1 more

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In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.2field-weighted citation impact, top 41% 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

13 citing papers in PubMed, 19 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

11 authors at 4 institutions in 1 country.

Yung-Li YangDepartments of Laboratory Medicine, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan.
Ching-Tzu YenDepartments of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Chen-Hsueh PaiDepartments of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Hsuan-Yu ChenInstitute of Statistical Science, Academia Sinica, Taipei, Taiwan.
Sung-Liang YuDepartments of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Chien-Yu LinInstitute of Statistical Science, Academia Sinica, Taipei, Taiwan.
Chung-Yi HuDepartments of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Shiann-Tarng JouDepartments of Pediatrics, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan.
Dong-Tsamn LinDepartments of Laboratory Medicine, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan.
Shu-Rung LinDepartment of Bioscience Technology, College of Science, Chung-Yuan Christian University, Taoyuan, Taiwan.
Shu-Wha LinDepartments of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Taipei, Taiwan.
National Taiwan University · TWNational Taiwan University Hospital · TWInstitute of Statistical Science, Academia Sinica · TWChung Yuan Christian University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Childhood acute lymphoblastic leukemia (ALL) with t(12;21), which results in expression of the ETV6/RUNX1 fusion gene, is the most common chromosomal lesion in precursor-B (pre-B) ALL. We identified 17 microRNAs that were downregulated in ETV6/RUNX1+ compared with ETV6/RUNX1- clinical samples. Among these microRNAs, miR-181a-1 was the most significantly reduced (by ~75%; P < 0.001). Using chromatin immunoprecipitation, we demonstrated that ETV6/RUNX1 directly binds the regulatory region of MIR181A1, and knockdown of ETV6/RUNX1 increased miR-181a-1 level. We further showed that miR-181a (functional counterpart of miR-181a-1) could target ETV6/RUNX1 and cause a reduction in the level of the oncoprotein ETV6/RUNX1, cell growth arrest, an increase in apoptosis, and induction of cell differentiation in ETV6/RUNX1+ cell line. Moreover, ectopic expression of miR-181a also resulted in decreased CD10 hyperexpression in ETV6/RUNX1+ primary patient samples. Taken together, our results demonstrate that MIR181A1 and ETV6/RUNX1 regulate each other, and we propose that a double negative loop involving MIR181A1 and ETV6/RUNX1 may contribute to ETV6/RUNX1-driven arrest of differentiation in pre-B ALL.

Indexed as

Cell DifferentiationCell Line, TumorCell ProliferationCore Binding Factor Alpha 2 SubunitETS Translocation Variant 6 ProteinGene Expression Regulation, LeukemicGene Knockdown TechniquesHumansMicroRNAsOncogene Proteins, FusionPrecursor Cell Lymphoblastic Leukemia-LymphomaProto-Oncogene Proteins c-etsRepressor ProteinsTranslocation, GeneticCore Binding Factor Alpha 2 SubunitETS Translocation Variant 6 ProteinMicroRNAsMIrn181 microRNA, humanOncogene Proteins, FusionProto-Oncogene Proteins c-etsRepressor ProteinsRUNX1 protein, human

Identifiers

PMID26580398
PMCPMC4651427
OpenAlexW2276771130

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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.