Evidence map›Paper›PMID 25757558›Full record

ArticleRNA biology2015

Transcriptional regulation of microRNA-100, -146a, and -150 genes by p53 and NFκB p65/RelA in mouse striatal STHdh(Q7)/ Hdh(Q7) cells and human cervical carcinoma HeLa cells.

Jayeeta Ghose, N P Bhattacharyya

Open access · bronzeAbstract read
In one paragraph

Article in RNA biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. 17β-estradiol promotes extracellular vesicle release and selective miRNA loading in ERα-positive breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
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

2 authors at 2 institutions in 2 countries.

Jayeeta Ghosea Crystallography and Molecular Biology Division; Saha Institute of Nuclear Physics ; Bidhannagar, Kolkata , India.
N P Bhattacharyya
Institute of Crystallography · ITSaha Institute of Nuclear Physics · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNA (miRNA) genes generally share many features common to those of protein coding genes. Various transcription factors (TFs) and co-regulators are also known to regulate miRNA genes. Here we identify novel p53 and NFκB p65/RelA responsive miRNAs and demonstrate that these 2 TFs bind to the regulatory sequences of miR-100, -146a and -150 in both mouse striatal and human cervical carcinoma cells and regulate their expression. p53 represses the miRNAs while NFκB p65/RelA induces them. Further, we provide evidence that exogenous p53 inhibits NFκB p65/RelA activity by reducing its nuclear content and competing with it for CBP binding. This suggests for the existence of a functional cross-talk between the 2 TFs in regulating miRNA expression. Moreover, promoter occupancy assay reveals that exogenous p53 excludes NFκB p65/RelA from its binding site in the upstream sequence of miR-100 gene thereby causing its repression. Thus, our work identifies novel p53 and NFκB p65/RelA responsive miRNAs in human and mouse and uncovers possible mechanisms of co-regulation of miR-100. It is to be mentioned here that cross-talks between p53 and NFκB p65/RelA have been observed to define the outcome of several biological processes and that the pro-apoptotic effect of p53 and the pro-survival functions of NFκB can be largely mediated via the biological roles of the miRNAs these TFs regulate. Our observation with cell lines thus provides an important platform upon which further work is to be done to establish the biological significance of such co-regulation of miRNAs by p53 and NFκB p65/RelA.

Indexed as

Gene Expression RegulationAnimalsCell Line, TumorHeLa CellsHumansMiceMicroRNAsPromoter Regions, GeneticTranscription Factor RelATumor Suppressor Protein p53MicroRNAsMIR150, humanMIRN100 microRNA, humanMIRN146 microRNA, humanTranscription Factor RelATumor Suppressor Protein p53ChIP, Chromatin immunoprecipitationCo-IP, Co-immunoprecipitationmicroRNAmiR-100miR-146amiR-150miRNA gene regulationmiRNAs, microRNAsNFκB, nuclear factor kappa-light-chain-enhancer of activated B cellsNFκB p65/RelAp53p53, tumor protein 53p65, RELA, RELARLU, Relative light unitRNA POL III, RNA Polymerase IIIRNA POL II, RNA Polymerase IIRT-PCR, Reverse transcription polymerase chain reactionTFBSTF, Transcriptional factortranscription factorTranscription factor binding sitev-rel avian reticuloendotheliosis viral oncogene homolog AWB, Western blot

Identifiers

PMID25757558
PMCPMC4615384
OpenAlexW1590964273

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.