Evidence map›Paper›PMID 17103045›Full record

ArticleJournal of bioenergetics and biomembranes2006

Multiple interference of the human papillomavirus-16 E7 oncoprotein with the functional role of the metastasis suppressor Nm23-H1 protein.

Anna Maria Mileo, Emanuela Piombino, Anna Severino, Alessandra Tritarelli, Marco G Paggi, Daniela Lombardi

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Journal of bioenergetics and biomembranes, 2006. 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
1.2field-weighted citation impact, top 23% 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, 36 citations in OpenAlex.

  1. NucleariScience · 2024
    Article
  2. Article
  3. Review
  4. Review
  5. Oncogenic Epstein-Barr virus recruits Nm23-H1 to regulate chromatin modifiers.Laboratory investigation; a journal of technical methods and pathology · 2018
    Review
  6. Article
  7. Review
  8. Regulation of the metastasis suppressor Nm23-H1 by tumor viruses.Naunyn-Schmiedeberg's archives of pharmacology · 2015
    Review
  9. Review
  10. Review
  11. Infection, mutation, and cancer evolution.Journal of molecular medicine (Berlin, Germany) · 2012
    Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Nucleoside diphosphate kinase/Nm23 and Epstein-Barr virus.Molecular and cellular biochemistry · 2009
    Review
  18. Clinical-translational approaches to the Nm23-H1 metastasis suppressor.Clinical cancer research : an official journal of the American Association for Cancer Research · 2008
    Review
  19. 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

6 authors at 2 institutions in 3 countries.

Anna Maria MileoDepartment for the Development of Therapeutic Programs, Laboratory C, Regina Elena Cancer Institute, Centre for Experimental Research, Via delle Messi d'Oro 156, 00158, Rome, Italy.
Emanuela Piombino
Anna Severino
Alessandra Tritarelli
Marco G Paggi
Daniela Lombardi
Centre of Experimental Medicine of the Slovak Academy of Sciences · SKUniversity of L'Aquila · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High-risk human papillomaviruses (HPV) are linked to human cervical and other ano-genital cancers. Integration of the viral genome in the transformed epithelial cells is restricted to the coding regions for the E6 and E7 oncoproteins. Nevertheless, E7 plays the major role in cell transformation. We report a novel interaction between HPV-16 E7 and the Nm23-H1 and Nm23-H2 proteins identified in yeast by the two-hybrid system and confirmed by co-immunoprecipitation in the human keratinocyte HaCaT cell line. Expression of the E7 oncoprotein in HaCaT cells induces modified keratinocyte proliferation and differentiation patterns, and leads to down-modulation and functional inactivation of the metastasis suppressor Nm23-H1 protein. Both transcriptional down-regulation and protein degradation contribute to reduce Nm23-H1 intracellular content. Besides metastasis suppression, Nm23-H1 displays multiple functions in cell cycle regulation and differentiation, development, DNA regulation and caspase-independent apoptosis. As a consequence of Nm23-H1 inhibition, HPV-16 E7 expressing HaCaT cells, acquire invasiveness capabilities and resistance to granzyme A-induced apoptosis. We propose that impairment of the multifunctional role of Nm23-H1 is an important feature consistent with the complex strategy carried out by HPV-16 E7 to promote cell transformation and tumor progression.

Indexed as

Gene Expression Regulation, NeoplasticGenes, Tumor SuppressorBlotting, WesternCell DifferentiationCell LineCell Transformation, NeoplasticFlow CytometryGlutathione TransferaseHuman papillomavirus 16HumansImmunoprecipitationKeratinocytesNeoplasmsNM23 Nucleoside Diphosphate KinasesNucleoside-Diphosphate KinaseOncogene Proteins, ViralGlutathione TransferaseNM23 Nucleoside Diphosphate KinasesNME1 protein, humanNucleoside-Diphosphate Kinaseoncogene protein E7, Human papillomavirus type 16Oncogene Proteins, ViralPapillomavirus E7 Proteins

Identifiers

PMID17103045
OpenAlexW2045588560

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.