Evidence map›Paper›PMID 25737447›Full record

ArticleThe Journal of biological chemistry2015

MicroRNA-31 is a transcriptional target of histone deacetylase inhibitors and a regulator of cellular senescence.

Joon-Ho Cho, Manjari Dimri, Goberdhan P Dimri

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 83 citations in OpenAlex.

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  11. Host gene and its guest: short story about relation of long-noncodingReports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology · 2023
    Review
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  18. Epigenetic dynamics in cancer stem cell dormancy.Cancer metastasis reviews · 2020
    Review
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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

3 authors at 1 institution in 1 country.

Joon-Ho ChoFrom the Department of Biochemistry and Molecular Medicine, School of Medicine and Health Sciences, The George Washington University, Washington, D. C.
Manjari DimriFrom the Department of Biochemistry and Molecular Medicine, School of Medicine and Health Sciences, The George Washington University, Washington, D. C. mdimri@gwu.edu.
Goberdhan P DimriFrom the Department of Biochemistry and Molecular Medicine, School of Medicine and Health Sciences, The George Washington University, Washington, D. C. gdimri@gwu.edu.
George Washington University · US

Funding

The role of BMI1 in breast cancerR01CA094150 · NCI · NORTHSHORE UNIV HEALTHSYSTEM RES INST · PI DIMRI, GOBERDHAN P · 2003 to 2013
$2.7M
NCI NIH HHS R01 CA094150
6 · The paper itself

Abstract

MicroRNAs (miRNAs) have emerged as important regulators of tumorigenesis. Several miRNAs, which can function either as oncomiRs or tumor suppressive miRs are deregulated in cancer cells. The microRNA-31 (miR-31) has been shown to be overexpressed in metastatic breast cancer. It promotes multiple oncogenic phenotypes, including proliferation, motility, and invasion of cancer cells. Using a breast cancer-related miRNA array analysis, we identified miR-31 as a novel target of histone deacetylase inhibitors (HDACi) in breast cancer cells. Specifically, we show that sodium butyrate (NaB) and panobinostat (LBH589), two broad-spectrum HDAC inhibitors up-regulate hsa-miR-31 (miR-31). The up-regulation of miR-31 was accompanied by repression of the polycomb group (PcG) protein BMI1 and induction of cellular senescence. We further show that inhibition of miR-31 overcomes the senescence-inducing effect of HDACi, and restores expression of the PcG protein BMI1. Interestingly, BMI1 also acts as a repressor of miR-31 transcription, suggesting a cross-negative feedback loop between the expression of miR-31 and BMI1. Our data suggest that miR-31 is an important physiological target of HDACi, and that it is an important regulator of senescence relevant to cancer. These studies further suggest that manipulation of miR-31 expression can be used to modulate senescence-related pathological conditions such as cancer, and the aging process.

Indexed as

Gene Expression Regulation, NeoplasticApoptosisButyric AcidCell Line, TumorCellular SenescenceFeedback, PhysiologicalFemaleHistone Deacetylase InhibitorsHumansHydroxamic AcidsIndolesMCF-7 CellsMicroarray AnalysisMicroRNAsOligonucleotide Array Sequence AnalysisPanobinostatBMI1 protein, humanButyric AcidHistone Deacetylase InhibitorsHydroxamic AcidsIndolesMicroRNAsMIRN31 microRNA, humanPanobinostatPolycomb Repressive Complex 1bmi1Breast CancerHistone Deacetylase Inhibitor (HDAC Inhibitor) (HDI)MicroRNA (miRNA)PolycombSenescence

Identifiers

PMID25737447
PMCPMC4400362
OpenAlexW2002853429

What OpenQuestion holds

Textmetadata
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.