Evidence map›Paper›PMID 26517243›Full record

ArticleOncotarget2015

Epigenetic silencing of tumor suppressor miR-3151 contributes to Chinese chronic lymphocytic leukemia by constitutive activation of MADD/ERK and PIK3R2/AKT signaling pathways.

Lu Qian Wang, Kwan Yeung Wong, Anders Rosèn, Chor Sang Chim

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
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

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. MircoRNAs predict and modulate responses to chemotherapy in leukemic patients.Naunyn-Schmiedeberg's archives of pharmacology · 2025
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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

4 authors at 3 institutions in 3 countries.

Lu Qian WangDepartment of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong.
Kwan Yeung WongDepartment of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong.
Anders RosènDepartment of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
Chor Sang ChimDepartment of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong.
Queen Mary Hospital · CNLinköping University · SEUniversity of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We hypothesize that miR-3151, localized to a GWAS-identified chronic lymphocytic leukemia (CLL) risk locus (8q22.3), is a tumor suppressor miRNA silenced by promoter DNA methylation in CLL. The promoter of miR-3151 was methylated in 5/7 (71%) CLL cell lines, 30/98 (31%) diagnostic primary samples, but not normal controls. Methylation of miR-3151 correlated inversely with expression. Treatment with 5-Aza-2'-deoxycytidine led to promoter demethylation and miR-3151 re-expression. Luciferase assay confirmed MAP-kinase activating death domain (MADD) and phosphoinositide-3-kinase, regulatory subunit 2 (PIK3R2) as direct targets of miR-3151. Moreover, restoration of miR-3151 resulted in inhibition of cellular proliferation and enhanced apoptosis, repression of MADD and PIK3R2, downregulation of MEK/ERK and PI3K/AKT signaling, and repression of MCL1. Lastly, miR-3151 methylation was significantly associated with methylation of miR-203 and miR-34b/c in primary CLL samples. Therefore, this study showed that miR-3151 is a tumor suppressive miRNA frequently hypermethylated and hence silenced in CLL. miR-3151 silencing by DNA methylation protected CLL cells from apoptosis through over-expression of its direct targets MADD and PIK3R2, hence constitutive activation of MEK/ERK and PI3K/AKT signaling respectively, and consequently over-expression of MCL1.

Indexed as

DNA MethylationEpigenesis, GeneticGene Silencing3' Untranslated RegionsAdultAgedAged, 80 and overApoptosisAsian PeopleAzacitidineBinding SitesCell Line, TumorCell ProliferationChinaDeath Domain Receptor Signaling Adaptor ProteinsDecitabine3' Untranslated RegionsAzacitidineDeath Domain Receptor Signaling Adaptor ProteinsDecitabineDNA Modification MethylasesEnzyme InhibitorsExtracellular Signal-Regulated MAP KinasesGuanine Nucleotide Exchange FactorsMADD protein, humanMCL1 protein, humanMicroRNAsMIRN203 microRNA, humanMIRN3151 microRNA, humanMIRN34 microRNA, humanMyeloid Cell Leukemia Sequence 1 ProteinPhosphatidylinositol 3-Kinasesphosphoinositol-3 kinase regulatory subunit 2, humanProto-Oncogene Proteins c-aktchronic lymphocytic leukemiaDNA methylationmicroRNAmiR-3151tumor suppressor

Identifiers

PMID26517243
PMCPMC4792566
OpenAlexW2242179450

What OpenQuestion holds

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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.