Evidence map›Paper›PMID 24336073›Full record

ArticleCell death & disease2013

miR-16 and miR-26a target checkpoint kinases Wee1 and Chk1 in response to p53 activation by genotoxic stress.

L Lezina, N Purmessur, A V Antonov, T Ivanova, E Karpova, K Krishan, M Ivan, V Aksenova, D Tentler, A V Garabadgiu and 2 more

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

Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.5field-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, 81 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

12 authors at 4 institutions in 4 countries.

L Lezina1] Molecular Pharmacology laboratory, Saint-Petersburg Institute of Technology, Saint-Petersburg 190013, Russia [2] Department of Biochemistry, University of Leicester, Leicester LE1 9HN, UK.
N PurmessurDepartment of Biochemistry, University of Leicester, Leicester LE1 9HN, UK.
A V AntonovMRC Toxicology Unit, Leicester LE1 9HN, UK.
T IvanovaDepartment of Biochemistry, University of Leicester, Leicester LE1 9HN, UK.
E KarpovaDepartment of Biochemistry, University of Leicester, Leicester LE1 9HN, UK.
K KrishanDepartment of Medicine, Indiana University, Indianapolis, IN 46202, USA.
M IvanDepartment of Medicine, Indiana University, Indianapolis, IN 46202, USA.
V AksenovaMolecular Pharmacology laboratory, Saint-Petersburg Institute of Technology, Saint-Petersburg 190013, Russia.
D TentlerMolecular Pharmacology laboratory, Saint-Petersburg Institute of Technology, Saint-Petersburg 190013, Russia.
A V GarabadgiuMolecular Pharmacology laboratory, Saint-Petersburg Institute of Technology, Saint-Petersburg 190013, Russia.
G Melino1] Molecular Pharmacology laboratory, Saint-Petersburg Institute of Technology, Saint-Petersburg 190013, Russia [2] MRC Toxicology Unit, Leicester LE1 9HN, UK [3] Faculty of Medicine, University of Rome 'Tor Vergata', Rome 00133, Italy.
N A Barlev1] Molecular Pharmacology laboratory, Saint-Petersburg Institute of Technology, Saint-Petersburg 190013, Russia [2] Department of Biochemistry, University of Leicester, Leicester LE1 9HN, UK [3] Gene Expression Laboratory, Institute of Cytology, Saint-Petersburg 194064, Russia.
St. Petersburg State Technological Institute · RUUniversity of Leicester · GBIndiana University – Purdue University Indianapolis · USMRC Toxicology Unit · GB

Funding

Medical Research Council MC_U132670600
6 · The paper itself

Abstract

The tumour suppressor p53 is a crucial regulator of cell cycle arrest and apoptosis by acting as a transcription factor to regulate a variety of genes. At least in part, this control is exerted by p53 via regulating expression of numerous microRNAs. We identified two abundantly expressed microRNAs, miR-16 and miR-26a, whose expression is regulated by p53 during the checkpoint arrest induced by the genotoxic drug, doxorubicin. Importantly, among the targets of these miRs are two critical checkpoint kinases, Chk1 and Wee1. The p53-dependent augmentation of miR-16 and miR-26a expression levels led to the cell cycle arrest of tumour cells in G1/S and increased apoptosis. Strikingly, the bioinformatics analysis of survival times for patients with breast and prostate cancers has revealed that co-expression of mir-16 and miR-26a correlated with a better survival outcome. Collectively, our data provide a novel mechanism whereby p53 represses Chk1 and Wee1 expression, at least partially, via upregulation of miR-16 and miR-26a and thus sensitizes tumour cells to genotoxic therapies.

Indexed as

Blotting, WesternCell CycleCell Cycle CheckpointsCell Cycle ProteinsCell Line, TumorCheckpoint Kinase 1Chromatin ImmunoprecipitationDNA DamageHumansMicroRNAsNuclear ProteinsProtein KinasesProtein-Tyrosine KinasesTumor Suppressor Protein p53Cell Cycle ProteinsCheckpoint Kinase 1CHEK1 protein, humanMicroRNAsMIRN16 microRNA, humanMIRN26 microRNA, humanNuclear ProteinsProtein KinasesProtein-Tyrosine KinasesTumor Suppressor Protein p53WEE1 protein, human

Identifiers

PMID24336073
PMCPMC3877554
OpenAlexW2003933871

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.