Evidence map›Paper›PMID 33073700›Full record

ArticleTechnology in cancer research & treatment

Oncogenic Long Noncoding RNA DARS-AS1 in Childhood Acute Myeloid Leukemia by Binding to microRNA-425.

Binghua Dou, Zhu Jiang, Xiaoguang Chen, Chunmei Wang, Jing Wu, Jindou An, Guangyao Sheng

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

Article in Technology in cancer research & treatment. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 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

7 authors at 2 institutions in 1 country.

Binghua DouDepartment of Paediatrics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, People's Republic of China.
Zhu JiangDepartment of Ultrasound, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, People's Republic of China.
Xiaoguang ChenDepartment of Paediatrics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, People's Republic of China.
Chunmei WangDepartment of Paediatrics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, People's Republic of China.
Jing WuDepartment of Paediatrics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, People's Republic of China.
Jindou AnDepartment of Paediatrics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, People's Republic of China.
Guangyao ShengDepartment of Paediatrics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, People's Republic of China.ORCID 0000-0002-1756-5257
First Affiliated Hospital of Zhengzhou University · CNThird Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveAcute myeloid leukemia (AML) represents a hematological cancer. The aim of the investigation was to probe the regulatory relevance of long non-coding RNA (lncRNA) aspartyl-tRNA synthetase anti-sense 1 (DARS-AS1)/microRNA-425 (miR-425)/transforming growth factor-beta 1 (TGFB1) to the development of AML.

methodsThe DARS-AS1 expression in bone marrow tissues was first analyzed in healthy subjects and AML patients. Subsequently, AML cell lines with DARS-AS1 knockdown were constructed, followed by cell proliferation and apoptosis assays. Afterward, downstream miRNA of DARS-AS1 and target mRNA of the miRNA were analyzed by bioinformatics, and their binding relationships were verified. Functional rescue experiments were then implemented. Finally, activation of the Smad2/3 signaling in MV4-11 and BF-24 cells were detected by western blot.

resultsDARS-AS1 was overexpressed in bone marrow tissues of AML patients and cells, and DARS-AS1 knockdown suppressed the proliferation of AML cells and induced apoptosis. DARS-AS1 bound to and negatively correlated with miR-425. Further results suggested that TGFB1 might be a target gene of miR-425 and could promote Smad2/3 phosphorylation and nuclear translocation. Finally, DARS-AS1 depletion could diminish the tumor volume

conclusionAll in all, we highlighted here that DARS-AS1 enhanced the expression of TGFB1 through binding to miR-425 to modulate AML progression via the Smad2/3 pathway, which might perform as a therapeutic target for AML.

Indexed as

AdolescentApoptosisCarcinogenesisCell Line, TumorCell MovementCell ProliferationChildChild, PreschoolFemaleGene Expression Regulation, NeoplasticHumansInfantLeukemia, Myeloid, AcuteMaleMicroRNAsRNA, Long NoncodingMicroRNAsMIRN425 microRNA, humanRNA, Long NoncodingSmad2 ProteinTGFB1 protein, humanTransforming Growth Factor beta1acute myeloid leukemiaDARS-AS1microRNA-425Smad2/3 signalingTGFB1

Identifiers

PMID33073700
PMCPMC7592321
OpenAlexW3093176363

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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.