Evidence map›Paper›PMID 29120412›Full record

ArticleCell death & disease2017

Bortezomib-induced miRNAs direct epigenetic silencing of locus genes and trigger apoptosis in leukemia.

Yu-Yi Chu, Chiung-Yuan Ko, Shao-Ming Wang, Pin-I Lin, Han-Ying Wang, Wen-Chi Lin, Dong-Yu Wu, Lu-Hao Wang, Ju-Ming Wang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

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  12. Dual Role of YY1 in HPV Life Cycle and Cervical Cancer Development.International journal of molecular sciences · 2022
    Review
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  18. Effect of Bortezomib on Global Gene Expression in PC12-Derived Nerve Cells.International journal of molecular sciences · 2020
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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

9 authors at 2 institutions in 1 country.

Yu-Yi ChuInstitute of Bioinformatics and Biosignal Transduction, National Cheng Kung University, Tainan, Taiwan.
Chiung-Yuan KoThe Ph.D. Program for Neural Regenerative Medicine, Taipei Medical University, Taipei, Taiwan.
Shao-Ming WangInstitute of Basic Medical Sciences, National Cheng Kung University, Tainan, Taiwan.
Pin-I LinInstitute of Bioinformatics and Biosignal Transduction, National Cheng Kung University, Tainan, Taiwan.
Han-Ying WangInstitute of Bioinformatics and Biosignal Transduction, National Cheng Kung University, Tainan, Taiwan.
Wen-Chi LinDepartment of Biotechnology and Bioindustry Sciences, College of Bioscience and Biotechnology, National Cheng Kung University, Tainan, Taiwan.
Dong-Yu WuInstitute of Bioinformatics and Biosignal Transduction, National Cheng Kung University, Tainan, Taiwan.
Lu-Hao WangInstitute of Bioinformatics and Biosignal Transduction, National Cheng Kung University, Tainan, Taiwan.
Ju-Ming WangInstitute of Bioinformatics and Biosignal Transduction, National Cheng Kung University, Tainan, Taiwan.
National Cheng Kung University · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) have been suggested to repress transcription via binding the 3'-untranslated regions of mRNAs. However, the involvement and details of miRNA-mediated epigenetic regulation, particularly in targeting genomic DNA and mediating epigenetic regulation, remain largely uninvestigated. In the present study, transcription factor CCAAT/enhancer binding protein delta (CEBPD) was responsive to the anticancer drug bortezomib, a clinical and highly selective drug for leukemia treatment, and contributed to bortezomib-induced cell death. Interestingly, following the identification of CEBPD-induced miRNAs, we found that miR-744, miR-3154 and miR-3162 could target CpG islands in the 5'-flanking region of the CEBPD gene. We previously demonstrated that the Yin Yang 1 (YY1)/polycomb group (PcG) protein/DNA methyltransferase (DNMT) complex is important for CCAAT/enhancer binding protein delta (CEBPD) gene inactivation; we further found that Argonaute 2 (Ago2) interacts with YY1 and binds to the CEBPD promoter. The miRNA/Ago2/YY1/PcG group protein/DNMT complex linked the inactivation of CEBPD and genes adjacent to its 5'-flanking region, including protein kinase DNA-activated catalytic polypeptide (PRKDC), minichromosome maintenance-deficient 4 (MCM4) and ubiquitin-conjugating enzyme E2 variant 2 (UBE2V2), upon bortezomib treatment. Moreover, we revealed that miRNA binding is necessary for YY1/PcG group protein/DNMT complex-mediated epigenetic gene silencing and is associated with bortezomib-induced methylation on genomic DNA. The present study successfully characterized the interactions of the miRNA/Ago2/YY1/PcG group protein/DNMT complex and provided new insights for miRNA-mediated epigenetic regulation in bortezomib-induced leukemic cell arrest and cell death.

Indexed as

3' Untranslated RegionsAntineoplastic AgentsApoptosisArgonaute ProteinsBortezomibCCAAT-Enhancer-Binding Protein-deltaCell Line, TumorCpG IslandsDNA-Activated Protein KinaseDNA MethylationGene SilencingHumansLeukemiaLigasesMicroRNAsMinichromosome Maintenance Complex Component 43' Untranslated RegionsAGO2 protein, humanAntineoplastic AgentsArgonaute ProteinsBortezomibCCAAT-Enhancer-Binding Protein-deltaDNA-Activated Protein KinaseLigasesMCM4 protein, humanMicroRNAsMinichromosome Maintenance Complex Component 4Nuclear ProteinsPRKDC protein, humanUBE2V2 protein, humanUbiquitin-Conjugating EnzymesYY1 protein, humanYY1 Transcription Factor

Identifiers

PMID29120412
PMCPMC5775404
OpenAlexW2767252471

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.