Evidence map›Paper›PMID 22615843›Full record

ArticlePloS one2012

Interferon-β induces cellular senescence in cutaneous human papilloma virus-transformed human keratinocytes by affecting p53 transactivating activity.

Maria V Chiantore, Serena Vannucchi, Rosita Accardi, Massimo Tommasino, Zulema A Percario, Gabriele Vaccari, Elisabetta Affabris, Gianna Fiorucci, Giovanna Romeo

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. Trial
  2. Article
  3. p53 signaling in cancer progression and therapy.Cancer cell international · 2021
    Review
  4. Article
  5. Lack of Cell Cycle Inhibitor p21 and Low CD4Frontiers in immunology · 2021
    Article
  6. P53: A Guardian of Immunity Becomes Its Saboteur through Mutation.International journal of molecular sciences · 2020
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. p53 as an Effector or Inhibitor of Therapy Response.Cold Spring Harbor perspectives in medicine · 2015
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Maria V ChiantoreDepartment of Infectious, Parasitic and Immune-mediated Diseases, Istituto Superiore di Sanità, Rome, Italy.
Serena Vannucchi
Rosita Accardi
Massimo Tommasino
Zulema A Percario
Gabriele Vaccari
Elisabetta Affabris
Gianna Fiorucci
Giovanna Romeo
Istituto Superiore di Sanità · ITCentre International de Recherche sur le Cancer · FRInstitute of Molecular Biology and Pathology · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interferon (IFN)-β inhibits cell proliferation and affects cell cycle in keratinocytes transformed by both mucosal high risk Human Papilloma Virus (HPV) and cutaneous HPV E6 and E7 proteins. In particular, upon longer IFN-β treatments, cutaneous HPV38 expressing cells undergo senescence. IFN-β appears to induce senescence by upregulating the expression of the tumor suppressor PML, a well known IFN-induced gene. Indeed, experiments in gene silencing via specific siRNAs have shown that PML is essential in the execution of the senescence programme and that both p53 and p21 pathways are involved. IFN-β treatment leads to a modulation of p53 phosphorylation and acetylation status and a reduction in the expression of the p53 dominant negative ΔNp73. These effects allow the recovery of p53 transactivating activity of target genes involved in the control of cell proliferation. Taken together, these studies suggest that signaling through the IFN pathway might play an important role in cellular senescence. This additional understanding of IFN antitumor action and mechanisms influencing tumor responsiveness or resistance appears useful in aiding further promising development of biomolecular strategies in the IFN therapy of cancer.

Indexed as

Cell Transformation, ViralAcetylationCell CycleCell Growth ProcessesCells, CulturedCellular SenescenceGene SilencingHumansInterferon-betaKeratinocytesNuclear ProteinsPapillomaviridaePapillomavirus E7 ProteinsPhosphorylationPromyelocytic Leukemia ProteinProtein Processing, Post-TranslationalInterferon-betaNuclear ProteinsPapillomavirus E7 ProteinsPML protein, humanPromyelocytic Leukemia ProteinTrans-ActivatorsTranscription FactorsTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID22615843
PMCPMC3353995
OpenAlexW2083301581

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.