Evidence map›Paper›PMID 19014482›Full record

ArticleRetrovirology2008

MicroRNA miR-146a and further oncogenesis-related cellular microRNAs are dysregulated in HTLV-1-transformed T lymphocytes.

Klemens Pichler, Grit Schneider, Ralph Grassmann

Open access · goldAbstract read
In one paragraph

Article in Retrovirology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

66 citing papers in PubMed, 108 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. A Review of the Interaction between miRNAs and Ebola Virus.International journal of molecular and cellular medicine · 2024
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Regulation of HTLV-1 transformation.Bioscience reports · 2022
    Review
  11. Article
  12. microRNA-146a-5p, Neurotropic Viral Infection and Prion Disease (PrD).International journal of molecular sciences · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Mechanisms of Oncogenesis by HTLV-1 Tax.Pathogens (Basel, Switzerland) · 2020
    Review
  19. Review
  20. The Role of miRNAs in Virus-Mediated Oncogenesis.International journal of molecular sciences · 2018
    Review

6 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Klemens PichlerInstitute of Clinical and Molecular Virology, University Erlangen-Nuremberg, Schlossgarten 4, Erlangen, Germany. klemens.pichler@viro.med.uni-erlangen.de
Grit Schneider
Ralph Grassmann
Friedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHuman T-lymphotropic virus type 1 (HTLV-1) is the etiologic agent of a severe and fatal lymphoproliferative disease of mainly CD4+ T cell origin, adult T cell leukemia, which develops after prolonged viral persistence. Transformation of infected cells involves HTLV-1's oncoprotein Tax, which perturbs cell cycle regulation and modulates cellular gene expression. The latter function is also a hallmark of microRNAs, a rather new layer in the regulation of gene expression. Affecting e.g. proliferation, microRNAs constitute a potential target for viral interference on the way to persistence and transformation. Hence, we explored the interconnections between HTLV-1 and cellular microRNAs.

resultsWe report that several microRNAs--miRs 21, 24, 146a, 155 and 223--are deregulated in HTLV-1-transformed cells. They are all upregulated except for miR-223, which is downregulated. Each of those microRNAs has ties to cancer. Their expression pattern forms a uniform phenotype among HTLV-transformed cells when compared to HTLV-negative control cells. In particular, miR-146a expression was found to be directly stimulated by Tax via NF-kappaB-mediated transactivation of its promoter; a single NF-kappaB site proximal to the transcription start point was necessary and sufficient for this to happen. An in silico analysis of potential target genes revealed candidates that might be coregulated by two or more of the aforementioned overexpressed microRNAs.

conclusionThese data demonstrate that cellular microRNAs are deregulated in HTLV-1-transformed T cells. In the case of miR-146a, this could be directly attributed to HTLV's oncoprotein Tax. Interference with cellular microRNAs may be crucial to maintaining persistence or may facilitate transformation of host cells.

Indexed as

Cell Transformation, ViralGene Expression RegulationBinding SitesCell LineGene Products, taxHumansHuman T-lymphotropic virus 1MicroRNAsNF-kappa BProtein BindingT-LymphocytesGene Products, taxMicroRNAsNF-kappa Btax protein, Human T-lymphotrophic virus 1

Identifiers

PMID19014482
PMCPMC2628945
OpenAlexW2148993356

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.