Evidence map›Paper›PMID 24256616›Full record

ArticleBMC cancer2013

Identification of new p53 target microRNAs by bioinformatics and functional analysis.

Alessandra Bisio, Veronica De Sanctis, Valerio Del Vescovo, Michela A Denti, Anil G Jegga, Alberto Inga, Yari Ciribilli

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 10% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. The Emerging Roles of CircPVT1 in Cancer Progression.Current pharmaceutical biotechnology · 2025
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  10. Review
  11. Extracellular and Intracellular Factors in Brain Cancer.Frontiers in cell and developmental biology · 2021
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

7 authors at 2 institutions in 2 countries.

Alessandra BisioLaboratory of Transcriptional Networks, Center for Integrative Biology, CIBIO, University of Trento, Trento, Italy. ciribilli@science.unitn.it.
Veronica De Sanctis
Valerio Del Vescovo
Michela A Denti
Anil G Jegga
Alberto Inga
Yari Ciribilli
University of Trento · ITCincinnati Children's Hospital Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe tumor suppressor p53 is a sequence-specific transcription factor that regulates an extensive network of coding genes, long non-coding RNAs and microRNAs, that establish intricate gene regulatory circuits influencing many cellular responses beyond the prototypical control of cell cycle, apoptosis and DNA repair.

methodsUsing bioinformatic approaches, we identified an additional group of candidate microRNAs (miRs) under direct p53 transcriptional control. To validate p53 family-mediated responsiveness of the newly predicted target miRs we first evaluated the potential for wild type p53, p63β and p73β to transactivate from p53 response elements (REs) mapped in the miR promoters, using an established yeast-based assay.

resultsThe REs found in miR-10b, -23b, -106a, -151a, -191, -198, -202, -221, -320, -1204, -1206 promoters were responsive to p53 and 8 of them were also responsive to p63β or p73β. The potential for germline p53 mutations to drive transactivation at selected miR-associated REs was also examined. Chromatin Immuno-Precipitation (ChIP) assays conducted in doxorubicin-treated MCF7 cells and HCT116 p53+/+ revealed moderate induction of p53 occupancy at the miR-202, -1204, -1206, -10b RE-containing sites, while weak occupancy was observed for the miR-23b-associated RE only in MCF7 cells. RT-qPCR analyses cells showed modest doxorubicin- and/or Nutlin-dependent induction of the levels of mature miR-10b, -23b, -151a in HCT116 p53+/+ and MCF7 cells. The long noncoding RNA PVT1 comprising miR-1204 and -1206 was weakly induced only in HCT116 p53+/+ cells, but the mature miRs were not detected. miR-202 expression was not influenced by p53-activating stimuli in our cell systems.

conclusionsOur study reveals additional miRs, particularly miR-10b and miR-151a, that could be directly regulated by the p53-family of transcription factors and contribute to the tuning of p53-induced responses.

Indexed as

Gene Expression Regulation, NeoplasticAntibiotics, AntineoplasticBinding SitesChromatinComputational BiologyDNA-Binding ProteinsDoxorubicinGenes, ReporterHCT116 CellsHumansLuciferases, FireflyMCF-7 CellsMicroRNAsNuclear ProteinsPromoter Regions, GeneticProtein BindingAntibiotics, AntineoplasticChromatinDNA-Binding ProteinsDoxorubicinLuciferases, FireflyMicroRNAsNuclear ProteinsRNA, Long NoncodingTP53 protein, humanTP63 protein, humanTranscription FactorsTumor Protein p73Tumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID24256616
PMCPMC4225545
OpenAlexW2015059296

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.