Evidence map›Paper›PMID 30072211›Full record

ArticleEBioMedicine2018

The Long Noncoding RNA MEG3 and its Target miR-147 Regulate JAK/STAT Pathway in Advanced Chronic Myeloid Leukemia.

Zi-Ye Li, Lin Yang, Xiao-Jun Liu, Xing-Zhe Wang, Yu-Xia Pan, Jian-Min Luo

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

47 citing papers in PubMed, 91 citations in OpenAlex.

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  7. LncRNAiScience · 2024
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  15. Non-Coding RNAs Are Implicit in Chronic Myeloid Leukemia Therapy Resistance.International journal of molecular sciences · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Zi-Ye LiDepartment of Hematology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, China.
Lin YangDepartment of Hematology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, China.
Xiao-Jun LiuDepartment of Hematology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, China.
Xing-Zhe WangDepartment of Hematology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, China.
Yu-Xia PanDepartment of Hematology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, China.
Jian-Min LuoDepartment of Hematology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, China. Electronic address: zymhbsjz@163.com.
Hebei Medical University · CNSecond Hospital of Hebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLong non-coding (lnc) RNAs plays an important role in chronic myeloid leukemia (CML). In this study, we aimed to uncover the mechanism of the lncRNA maternally expressed 3 (MEG3) and its target microRNA-147 (miR-147) in CML.

methodsSixty CML patients and 10 healthy donors were included in the study. The methylation of MEG3 and miR-147 promoter was determined by methylation-specific PCR. The relationship of MEG3 and miR-147 was explored by luciferase assay. The interactions of proteins were studied by RNA pull-down assay, RNA immunoprecipitation and co-immunoprecipitation.

findingsPatients in accelerated phase CML (CML-AP) and blast phase CML (CML-BP) showed lower expressions of MEG3 and miR-147 and higher expressions of DNMT1, DNMT3B, MBD2, MECP2 and HDAC1 compared to the controls. These patients also showed a higher degree of methylation of MEG3 and miR-147 while there was a reduction after chidamide treatment. Furthermore, the overexpression of MEG3 and miR-147 inhibited cell proliferation both in vivo and in vitro, promoted apoptosis and decreased the expressions of DNMT1, DNMT3A, DNMT3B, MBD2, HDAC1 and MECP2. We also found MEG3 interacted with DNMT1, JAK2, STAT3, HDAC1, and TYK2, and JAK2 was bound to STAT3, STAT5 and MYC. More interestingly, JAK2 was bound to TYK2 by the bridge of MEG3.

interpretationLncRNA MEG3 and its target miR-147 may serve as a novel therapeutic target for CML blast crisis, and chidamide might have a potential clinical application in treating CML blast crisis.

Indexed as

AdolescentAdultAgedAnimalsCell Line, TumorChildFemaleHumansJanus Kinase 2Leukemia, Myelogenous, Chronic, BCR-ABL PositiveMaleMice, NudeMicroRNAsMiddle AgedRNA, Long NoncodingSignal TransductionJAK2 protein, humanJanus Kinase 2MEG3 non-coding RNA, humanMicroRNAsMIRN147 microRNA, humanRNA, Long NoncodingSTAT3 protein, humanSTAT3 Transcription FactorSTAT5 Transcription FactorChidamideChronic myeloid leukemia blast crisislncRNA MEG3miR147 and epigenetic

Identifiers

PMID30072211
PMCPMC6117736
OpenAlexW2886416438

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.