Evidence map›Paper›PMID 21093004›Full record

ArticleVirology2011

Epstein-Barr Virus nuclear antigen 1 (EBNA1) confers resistance to apoptosis in EBV-positive B-lymphoma cells through up-regulation of survivin.

Jie Lu, Masanao Murakami, Subhash C Verma, Qiliang Cai, Sabyasachi Haldar, Rajeev Kaul, Mariusz A Wasik, Jaap Middeldorp, Erle S Robertson

Abstract read
In one paragraph

Article in Virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.9field-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

53 citing papers in PubMed, 94 citations in OpenAlex.

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  17. Viruses in colorectal cancer.Molecular oncology · 2022
    Review
  18. Article
  19. EBNA1 inhibitors have potent and selective antitumor activity in xenograft models of Epstein-Barr virus-associated gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2021
    Article
  20. Cell death pathways and viruses: Role of microRNAs.Molecular therapy. Nucleic acids · 2021
    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

9 authors at 2 institutions in 2 countries.

Jie LuDepartment of Microbiology and Tumor Virology Program, Abramson Comprehensive Cancer Center, School of Medicine, University of Pennsylvania, 202E Johnson Pavilion, 3610 Hamilton Walk, Philadelphia, PA 19104, USA.
Masanao Murakami
Subhash C Verma
Qiliang Cai
Sabyasachi Haldar
Rajeev Kaul
Mariusz A Wasik
Jaap Middeldorp
Erle S Robertson
University of Pennsylvania · USVrije Universiteit Amsterdam · NL

Funding

Mechanisms of Action of LANA encoded by KSHVR01CA091792 · NCI · UNIVERSITY OF PENNSYLVANIA · PI ROBERTSON, ERLE S. · 2002 to 2011
$3.4M
Mechanism of KSHV reactivationR01DE017338 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI ROBERTSON, ERLE S · 2005 to 2007
$811k
Understanding the mechanism of KSHV latent DNA replicationR00CA126182 · NCI · UNIVERSITY OF NEVADA RENO · PI VERMA, SUBHASH C · 2009 to 2011
$740k
Understanding the mechanism of KSHV latent DNA replicationK99CA126182 · NCI · UNIVERSITY OF PENNSYLVANIA · PI VERMA, SUBHASH C · 2007 to 2008
$250k
NCI NIH HHS CA072510NCI NIH HHS CA091792NCI NIH HHS K99 CA126182NCI NIH HHS K99CA126182NCI NIH HHS R00 CA126182NCI NIH HHS R01 CA091792NIDCR NIH HHS DE017338NIDCR NIH HHS R01 DE017338
6 · The paper itself

Abstract

Resistance to apoptosis is an important component of the overall mechanism which drives the tumorigenic process. EBV is a ubiquitous human gamma-herpesvirus which preferentially establishes latent infection in viral infected B-lymphocytes. EBNA1 is typically expressed in most forms of EBV-positive malignancies and is important for replication of the latent episome in concert with replication of the host cells. Here, we investigate the effects of EBNA1 on survivin up-regulation in EBV-infected human B-lymphoma cells. We present evidence which demonstrates that EBNA1 forms a complex with Sp1 or Sp1-like proteins bound to their cis-element at the survivin promoter. This enhances the activity of the complex and up-regulates survivin. Knockdown of survivin and EBNA1 showed enhanced apoptosis in infected cells and thus supports a role for EBNA1 in suppressing apoptosis in EBV-infected cells. Here, we suggest that EBV encoded EBNA1 can contribute to the oncogenic process by up-regulating the apoptosis suppressor protein, survivin in EBV-associated B-lymphoma cells.

Indexed as

ApoptosisB-LymphocytesCell Line, TumorEpstein-Barr Virus Nuclear AntigensHerpesvirus 4, HumanHumansInhibitor of Apoptosis ProteinsMicrotubule-Associated ProteinsPromoter Regions, GeneticProtein Structure, TertiaryRNA InterferenceSp1 Transcription FactorSurvivinTranscriptional ActivationUp-RegulationBIRC5 protein, humanEBV-encoded nuclear antigen 1Epstein-Barr Virus Nuclear AntigensInhibitor of Apoptosis ProteinsMicrotubule-Associated ProteinsSp1 Transcription FactorSurvivin

Identifiers

PMID21093004
PMCPMC4287362
OpenAlexW2034601852

What OpenQuestion holds

Textmetadata
LicenceTDM
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.