Evidence map›Paper›PMID 21599968›Full record

ArticleVirology journal2011

HPV16 E2 could act as down-regulator in cellular genes implicated in apoptosis, proliferation and cell differentiation.

Eric Ramírez-Salazar, Federico Centeno, Karen Nieto, Armando Valencia-Hernández, Mauricio Salcedo, Efraín Garrido

Open access · goldAbstract read
In one paragraph

Article in Virology journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  6. Article
  7. Prevalence of the integration status for human papillomavirus 16 in esophageal carcinoma samples.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2018
    Article
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  9. Review
  10. Article
  11. Article
  12. Article
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  15. HPV related diseases in males: a heavy vaccine-preventable burden.Journal of preventive medicine and hygiene · 2013
    Review
  16. Article
  17. Article
  18. Article
  19. 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 4 institutions in 2 countries.

Eric Ramírez-SalazarDepartment of Genetics and Molecular Biology, CINVESTAV-IPN, Mexico City, Mexico.
Federico Centeno
Karen Nieto
Armando Valencia-Hernández
Mauricio Salcedo
Efraín Garrido
Center for Research and Advanced Studies of the National Polytechnic Institute · MXMexican Social Security Institute · MXNational Institute of Genomic Medicine · MXYo quiero Yo puedo · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHuman Papillomavirus (HPV) E2 plays several important roles in the viral cycle, including the transcriptional regulation of the oncogenes E6 and E7, the regulation of the viral genome replication by its association with E1 helicase and participates in the viral genome segregation during mitosis by its association with the cellular protein Brd4. It has been shown that E2 protein can regulate negative or positively the activity of several cellular promoters, although the precise mechanism of this regulation is uncertain. In this work we constructed a recombinant adenoviral vector to overexpress HPV16 E2 and evaluated the global pattern of biological processes regulated by E2 using microarrays expression analysis.

resultsThe gene expression profile was strongly modified in cells expressing HPV16 E2, finding 1048 down-regulated genes, and 581 up-regulated. The main cellular pathway modified was WNT since we found 28 genes down-regulated and 15 up-regulated. Interestingly, this pathway is a convergence point for regulating the expression of genes involved in several cellular processes, including apoptosis, proliferation and cell differentiation; MYCN, JAG1 and MAPK13 genes were selected to validate by RT-qPCR the microarray data as these genes in an altered level of expression, modify very important cellular processes. Additionally, we found that a large number of genes from pathways such as PDGF, angiogenesis and cytokines and chemokines mediated inflammation, were also modified in their expression.

conclusionsOur results demonstrate that HPV16 E2 has regulatory effects on cellular gene expression in HPV negative cells, independent of the other HPV proteins, and the gene profile observed indicates that these effects could be mediated by interactions with cellular proteins. The cellular processes affected suggest that E2 expression leads to the cells in to a convenient environment for a replicative cycle of the virus.

Indexed as

ApoptosisCell DifferentiationDown-RegulationGene Expression RegulationHost-Pathogen InteractionsAdenoviridaeCell LineDNA-Binding ProteinsGene ExpressionGene Expression ProfilingGenetic VectorsHuman papillomavirus 16HumansMicroarray AnalysisOncogene Proteins, ViralDNA-Binding ProteinsE2 protein, Human papillomavirus type 16Oncogene Proteins, Viral

Identifiers

PMID21599968
PMCPMC3127837
OpenAlexW2098222076

What OpenQuestion holds

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LicenceCC BY
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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.