Evidence map›Paper›PMID 23823647›Full record

ArticleRNA biology2013

The interplay of HuR and miR-3134 in regulation of AU rich transcriptome.

Shivani Sharma, Suneer Verma, Madavan Vasudevan, Subhasis Samanta, Jitendra K Thakur, Ritu Kulshreshtha

Open access · bronzeAbstract read
In one paragraph

Article in RNA biology, 2013. 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
1.6field-weighted citation impact, top 17% 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, 26 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Hallmarks of cancer and AU-rich elements.Wiley interdisciplinary reviews. RNA · 2017
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Clinical significance of HuR expression in human malignancy.Medical oncology (Northwood, London, England) · 2014
    Review
  16. Regulation of the mRNA half-life in breast cancer.World journal of clinical oncology · 2014
    Review
  17. 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 3 institutions in 2 countries.

Shivani SharmaDepartment of Biochemical Engineering and Biotechnology; Indian Institute of Technology; Delhi, India.
Suneer Verma
Madavan Vasudevan
Subhasis Samanta
Jitendra K Thakur
Ritu Kulshreshtha
Indian Institute of Technology Delhi · INNational Institute of Plant Genome Research · INCorvid Technologies (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs and AU Rich element (ARE)-mediated degradation of transcripts are thought to be two independent means of gene regulation at the post-transcriptional level. However, since their site of action is the same (3'UTR of mRNA), there exists a high probability that specific miRNAs may bind to AREs and, thus, interact with ARE-binding proteins (ARE-BPs) to regulate transcript levels. In this study, we have characterized AREs as potential targets of hsa-miR-3134. An analysis of the global gene expression profile of breast cancer cell line MCF7 overexpressing miR-3134 revealed the presence of at least one AUUUA element in the 3'-UTRs of 63% of miR-3134 regulated protein coding genes. Quantitative RT-PCR or 3'UTR luciferase assays show that miR-3134 mediates an up to 4-8-fold increase in the levels of ARE bearing transcripts-SOX9, VEGFA, and EGFR, while mutated miR-3134 shows a decreased effect. The miR-3134-mediated increase in transcript levels was unaffected by treatment with transcription inhibitor (actinomycin D), indicating that miR-3134 enhances transcript stability. To investigate a possible interplay between miR-3134 and a prototype ARE-BP, HuR, we compared their overexpression transcriptome profiles. Interestingly, up to 80% of miR-3134-regulated genes were also regulated by HuR. Overexpression studies of HuR alone or in combination with miR-3134 shows that wt miR-3134 but not a mutated miR-3134 promotes stabilization of HuR-regulated transcripts SOX9, VEGFA, and EGFR as confirmed by qRT-PCR or RNA-immunoprecipitation experiments. Overall, this report suggests that collaboration between ARE-binding microRNAs and ARE-binding proteins could be a general mechanism of 3'-UTR mediated regulation of gene expression in human cells.

Indexed as

AU Rich Elements3' Untranslated RegionsDactinomycinELAV ProteinsErbB ReceptorsFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMCF-7 CellsMicroRNAsSOX9 Transcription FactorTranscriptomeVascular Endothelial Growth Factor A3' Untranslated RegionsDactinomycinEGFR protein, humanELAV ProteinsErbB ReceptorsMicroRNAsSOX9 protein, humanSOX9 Transcription FactorVascular Endothelial Growth Factor AVEGFA protein, humanAU rich elementsBreast cancerHuRMicroRNAmiR-3134

Identifiers

PMID23823647
PMCPMC3817149
OpenAlexW1983048002

What OpenQuestion holds

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Registered trials

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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.