Evidence map›Paper›PMID 19966860›Full record

ArticleOncogene2010

Epstein-Barr virus encoded LMP1 downregulates TCL1 oncogene through miR-29b.

E Anastasiadou, F Boccellato, S Vincenti, P Rosato, I Bozzoni, L Frati, A Faggioni, C Presutti, P Trivedi

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.2field-weighted citation impact, top 7% 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, 69 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Cobomarsen, an Oligonucleotide Inhibitor of miR-155, Slows DLBCL Tumor Cell GrowthClinical cancer research : an official journal of the American Association for Cancer Research · 2021
    Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. MicroRNAs in Autoimmunity and Hematological Malignancies.International journal of molecular sciences · 2018
    Review
  12. MiRNA Dysregulation in Childhood Hematological Cancer.International journal of molecular sciences · 2018
    Review
  13. Review
  14. The Nefarious Nexus of Noncoding RNAs in Cancer.International journal of molecular sciences · 2018
    Review
  15. Review
  16. Non-coding RNA networks in cancer.Nature reviews. Cancer · 2018
    Review
  17. Article
  18. Review
  19. Over-expression of miR-10b in NPC patients: correlation with LMP1 and Twist1.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    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

9 authors at 2 institutions in 1 country.

E AnastasiadouDepartment of Experimental Medicine and Pathology, Istituto Pasteur-Fondazione Cenci-Bolognetti, La Sapienza University, Rome, Italy.
F Boccellato
S Vincenti
P Rosato
I Bozzoni
L Frati
A Faggioni
C Presutti
P Trivedi
Sapienza University of Rome · ITIstituto Pasteur · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epstein-Barr virus (EBV) encoded latent membrane protein 1 (LMP1) is noted for its transforming potential. Yet, it also acts as a cytostatic and growth-relenting factor in Burkitt's lymphoma (BL) cells. The underlying molecular mechanisms of the growth inhibitory property of LMP1 have remained largely unknown. In this study, we show that LMP1 negatively regulates a major oncogene, TCL1, in diffuse large B-cell lymphoma (DLBCL) and BL cells. MicroRNA (miR) profiling of LMP1 transfectants showed that among others, miR-29b, is upregulated. LMP1 diminished TCL1 by inducing miR-29b through C-terminus activation region 1 (CTAR1) and CTAR2. miR-29b locked nucleic acid (LNA) antisense oligonucleotide transfection into LMP1-expressing cells reduced miR-29b expression and consequently reconstituted TCL1, suggesting that LMP1 negatively regulates TCL1 through miR-29b upregulation. The miR-29b increase by LMP1 was due to an increase in the cluster pri-miR-29b1-a transcription, derived from human chromosome 7. Using pharmacological inhibitors, we found that p38 mitogen-activated protein kinase-activating function of LMP1 is important for this effect. The ability of LMP1 to negatively regulate TCL1 through miR-29b might underlie its B-cell lymphoma growth antagonistic property. As LMP1 is also important for B-cell transformation, we suggest that the functional dichotomy of this viral protein may depend on a combination of levels of its expression, lineage and differentiation of the target cells and regulation of miRs, which then directs the outcome of the cellular response.

Indexed as

Cell Line, TumorGene Expression RegulationHerpesvirus 4, HumanHumansLymphoma, B-CellMicroRNAsOncogenesProto-Oncogene ProteinsSignal TransductionViral Matrix ProteinsEBV-associated membrane antigen, Epstein-Barr virusMicroRNAsProto-Oncogene ProteinsTCL1A protein, humanViral Matrix Proteins

Identifiers

PMID19966860
OpenAlexW2078224598

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.