Evidence map›Paper›PMID 26001294›Full record

ArticleOncotarget2017

p63 drives invasion in keratinocytes expressing HPV16 E6/E7 genes through regulation of Src-FAK signalling.

Kirtiman Srivastava, Adam Pickard, Simon McDade, Dennis J McCance

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. 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
1.5field-weighted citation impact, top 19% 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, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. ΔNp63γ/SRC/Slug Signaling Axis Promotes Epithelial-to-Mesenchymal Transition in Squamous Cancers.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018
    Article
  12. A double dealing tale of p63: an oncogene or a tumor suppressor.Cellular and molecular life sciences : CMLS · 2018
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. HPV disease transmission protection and control.Microbial cell (Graz, Austria) · 2016
    Review
  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

4 authors at 2 institutions in 2 countries.

Kirtiman SrivastavaCentre for Cancer Research and Cell Biology, Queen's University Belfast, Belfast BT9 7BL, UK.
Adam PickardCentre for Cancer Research and Cell Biology, Queen's University Belfast, Belfast BT9 7BL, UK.
Simon McDadeCentre for Cancer Research and Cell Biology, Queen's University Belfast, Belfast BT9 7BL, UK.
Dennis J McCanceCentre for Cancer Research and Cell Biology, Queen's University Belfast, Belfast BT9 7BL, UK.
Queen's University Belfast · GBUniversity of New Mexico · US

Funding

Medical Research Council G1001692
6 · The paper itself

Abstract

Using microarray information from oro-pharyngeal data sets and results from primary human foreskin keratinocytes (HFK) expressing Human Papilloma Virus (HPV)-16 E6/E7 proteins, we show that p63 expression regulates signalling molecules which initiate cell migration such as Src and focal adhesion kinase (FAK) and induce invasion in 3D-organotypic rafts; a phenotype that can be reversed by depletion of p63. Knockdown of Src or FAK in the invasive cells restored focal adhesion protein paxillin at cell periphery and impaired the cell migration. In addition, specific inhibition of FAK (PF573228) or Src (dasatinib) activities mitigated invasion and attenuated the expression/activity of matrix metalloproteinase 14 (MMP14), a pivotal MMP in the MMP activation cascade. Expression of constitutively active Src in non-invasive HFK expressing E6/E7 proteins upregulated the activity of c-Jun and MMP14, and induced invasion in rafts. Depletion of Src, FAK or AKT in the invasive cells normalised the expression/activity of c-Jun and MMP14, thus implicating the Src-FAK/AKT/AP-1 signalling in MMP14-mediated extra-cellular matrix remodelling. Up-regulation of Src, AP-1, MMP14 and p63 expression was confirmed in oro-pharyngeal cancer. Since p63 transcriptionally regulated expression of many of the genes in this signalling pathway, it suggests that it has a central role in cancer progression.

Indexed as

Blotting, WesternCarcinoma, Squamous CellCell MovementDasatinibFluorescent Antibody TechniqueFocal Adhesion Kinase 1ForeskinHumansKeratinocytesMaleMatrix Metalloproteinase 14Oncogene Proteins, ViralOropharyngeal NeoplasmsPapillomavirus E7 ProteinsPapillomavirus InfectionsProtein Kinase Inhibitors6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-oneDasatinibE6 protein, Human papillomavirus type 16Focal Adhesion Kinase 1Matrix Metalloproteinase 14MMP14 protein, humanoncogene protein E7, Human papillomavirus type 16Oncogene Proteins, ViralPapillomavirus E7 ProteinsProtein Kinase InhibitorsProto-Oncogene Proteins c-junPTK2 protein, humanQuinolonesRepressor Proteinssrc-Family KinasesSulfonesTP63 protein, humanTranscription Factor AP-1Transcription FactorsTumor Suppressor ProteinsHPV16invasionMMP14p63Src

Identifiers

PMID26001294
PMCPMC5369957
OpenAlexW1886855631

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.