Evidence map›Paper›PMID 25486198›Full record

ArticleCell cycle (Georgetown, Tex.)2014

p53 shapes genome-wide and cell type-specific changes in microRNA expression during the human DNA damage response.

Hiroyoshi Hattori, Rekin's Janky, Wilfried Nietfeld, Stein Aerts, M Madan Babu, Ashok R Venkitaraman

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Aging and Protein Kinases.Advances in experimental medicine and biology · 2021
    Article
  7. Observational
  8. Revealing a human p53 universe.Nucleic acids research · 2018
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. The big player governs small world too.Cell cycle (Georgetown, Tex.) · 2014
    Article
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

6 authors at 5 institutions in 5 countries.

Hiroyoshi Hattoria University of Cambridge; Medical Research Council Cancer Unit; Hutchison/MRC Research Center ; Cambridge , UK.
Rekin's Janky
Wilfried Nietfeld
Stein Aerts
M Madan Babu
Ashok R Venkitaraman
KU Leuven · BEClinical Research Management · USHutchison/MRC Research Centre · GBMax Planck Institute for Molecular Genetics · DEMedical Research Council · GB

Funding

Medical Research Council G1001521Medical Research Council G1001522Medical Research Council MC_U105185859Medical Research Council MC_U105359877Medical Research Council MC_UU_12022/1Medical Research Council MC_UU_12022/8
6 · The paper itself

Abstract

The human DNA damage response (DDR) triggers profound changes in gene expression, whose nature and regulation remain uncertain. Although certain micro-(mi)RNA species including miR34, miR-18, miR-16 and miR-143 have been implicated in the DDR, there is as yet no comprehensive description of genome-wide changes in the expression of miRNAs triggered by DNA breakage in human cells. We have used next-generation sequencing (NGS), combined with rigorous integrative computational analyses, to describe genome-wide changes in the expression of miRNAs during the human DDR. The changes affect 150 of 1523 miRNAs known in miRBase v18 from 4-24 h after the induction of DNA breakage, in cell-type dependent patterns. The regulatory regions of the most-highly regulated miRNA species are enriched in conserved binding sites for p53. Indeed, genome-wide changes in miRNA expression during the DDR are markedly altered in TP53-/- cells compared to otherwise isogenic controls. The expression levels of certain damage-induced, p53-regulated miRNAs in cancer samples correlate with patient survival. Our work reveals genome-wide and cell type-specific alterations in miRNA expression during the human DDR, which are regulated by the tumor suppressor protein p53. These findings provide a genomic resource to identify new molecules and mechanisms involved in the DDR, and to examine their role in tumor suppression and the clinical outcome of cancer patients.

Indexed as

DNA RepairGenomeCell LineDNA DamageGene Expression RegulationGene Expression Regulation, NeoplasticGenome, HumanHumansMicroRNAsNeoplasmsOrgan SpecificityTumor Suppressor Protein p53MicroRNAsTumor Suppressor Protein p53AP-1, activator protein-1clinical outcomecomputational analysisDDR, DNA damage responseDNA damage responsedouble stranded DNA breaks, DSBsE2F1, transcription factor E2F1FoxM1, forkhead box protein M1ionizing radiation, IRmicro-RNAmiRNA, micro-RNAmisc RNA, miscellaneous RNAnext-generation sequencingNF-k B, nuclear factor-k BNGS, next-generation sequencingp53scRNA, small cytoplasmic RNAsnoRNA, small nucleolar RNAsnRNA, small nuclear RNATF, transcription factorTP53, tumour protein p53tRNA, transfer RNA

Identifiers

PMID25486198
PMCPMC4601526
OpenAlexW2057675824

What OpenQuestion holds

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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.